Columbia  ^nibersiitp 
in  tiic  €itp  of  J^eto  l^crfe 

CoUege  of  ^fjpsicians  anb  ^urgeong 


3^ef  erence  Hibrarp 


DISEASES   OF   THE    HEART 


BY  THE  SAME  AUTHOR. 

THE    SCIENCE    AND    ART 
OF    PRESCRIBING 

BY 

E.  H.    COLBECK,   M.D.    F.R.C.P.  (Lond.),    D.P.H.   (Cantab.), 

AND 

ARNOLD   CHAPLIN,    M.D.    M.R.C.P.    (Lond.) 

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SKIAGRAM    OF    THE   CHEST   SHOWING   THE    POSITION    OF   THE   HEART 
(Hugh  Walsham) 

The  numbers  i-6  arc  placed  on  the  posterior  surface  of  the  first  six  ribs  in  front. 


DISEASES 
OF     THE     HEART 

A     CLINICAL     TEXT-BOOK     FOR     THE     USE     OF 
STUDENTS     AND     PRACTITIONERS     OF     MEDICINE 


EDMUND     HENRY     COLBECK 

B.A.,  M.D.,  BC.  (Cantab.);  F.R.C.P.  (London);  D.P.H.  (Cantab.) 

PHYSICIAN    TO   OUT-PATIENTS   AT    THE    CITY    OF    LONEON    HOSPITAL   FOR   DISEASES 

OF   THE   CHEST,   VICTORIA    PARK,    E. 

PHYSICIAN    TO   THE    METROPOLITAN    DISPENSARY,    E.G. 

LATE    HOUSE    PHYSICIAN    AT    ST.    MARY's    HOSPITAL 

ETC.,    ETC. 


WITH     FORTY-THREE    ILLUSTRATIONS 


SECOND     EDITION.      REVISED     AND     ENLARGED 


W.    T.    KEENER    &    Co., 

90   WABASH    AVENUE 

CHICAGO 

1905 


X-y^Y^ 


TO 

SIR   WILLIAM    H.   BROADBENT,  Bart. 

M.D.  (LoND.),  F.R.S.,  F.R.C.P. 

PHYSICIAN   IN   ORDINARY  TO   H.R.H.    THE   PRINCE   OF   WALES 

CONSULTING   PHYSICIAN   TO   ST.    MARY'S   HOSPITAL,    AND   THE  LONDON   FEVER   HOSPITAL 

LATE   PRESIDENT   OF   CLINICAL,    MEDICAL,    NEUROLOGICAL,    AND   HARVEIAN   SOCIETIES 

WHOSE  TEACHING  HAS  DONE  SO  MUCH  TO 

ADVANCE  THE  CLINICAL  STUDY  OF 

DISEASES   OF  THE  HEART 

THIS  BOOK 

IS    RESPECTFULLY  AND  GRATEFULLY 

DEDICATED 


PREFACE    TO   THE    SECOND    EDITION. 

I  HAVE  taken  advantage  of  the  opportunity  afforded  by 
the  demand  for  a  Second  Edition  of  "  Diseases  of  the  Heart " 
to  make  a  few  corrections  in  the  text,  and  to  add  a  little  new- 
matter,  without  in  any  way  interfering  with  the  general 
arrangement  and  character  of  the  work. 

A  short  account  has  been  given  of  mechanical  strain  of 
the  heart,  and  of  the  Stokes-Adams'  syndrome ;  and  the 
description  of  the  treatment  of  chronic  valvular  disease  has 
been  somewhat  amplified. 

The  instrumental  determination  of  blood  pressure  which 
seems  likely  to  occupy  a  prominent  place  in  the  clinical 
investigation  of  cardio-vascular  disease  has  received  but 
scant  consideration ;  but  in  the  present  state  of  our  knowledge 
it  appeared  hardly  profitable  to  enter  into  a  detailed 
description  of  this  method  of  procedure. 

The  remaining  additions  that  have  been  made  do  not  call 
for  comment,  but  it  is  hoped  that  they  may  enhance  what- 
ever usefulness  the  work  may  possess  as  a  clinical  guide  to 
diseases  of  the  heart. 

E.  H.  C. 

November  1904. 


PREFACE 

My  interest  in  Diseases  of  the  Heart  dates  from  the  time 
that  I  was  appointed  House  Physician  to  Sir  William 
Broadbent.  I  should  have  profited  more  by  the  leaching 
of  this  great  master  of  clinical  medicine  had  I  possessed 
a  better  knowledge  of  the  elementary  and  fundamental 
bedside  features  of  cardio-vascular  disease.  It  seemed  to 
me  at  this  time,  and  it  does  so  still,  that  a  book  dealing  with 
the  clinical  side  of  the  subject  of  Heart  Disease  in  a  form 
suitable  to  the  requirements  of  the  student  and  newly 
qualified  practitioner  of  medicine,  would  prove  of  very  great 
service. 

It  has  been  my  endeavour  in  the  following  pages  to  fulfil 
these  conditions  in  as  concise  and  systematic  a  manner  as 
possible.  In  order  to  keep  the  size  of  the  book  within 
reasonable  limits,  compression  of  the  subject-matter  was 
unavoidable ;  but  it  is  hoped  that  this  process  has  not  been 
carried  so  far  as  to  interfere  with  the  intelligibility  of  the 
text. 

Controversial  matter  has  to  a  large  extent  been  avoided, 
and  while  this  has  entailed  the  exclusion  of  much  new 
and  interesting  work,  it  has  also  permitted  of  much  greater 
precision  in  the  exposition  of  the  subject,  a  feature  of  no 
small  advantage  to  the  student  of  clinical  medicine. 

I  have  freely  consulted  and  made  use  of  the  writings  of 
the  leading  authorities  on  Diseases  of  the  Heart,  and  more 


PREFACE  ix 

particularly  those  of  Walshe,  Peacock,  Gairdner,  Balfour, 
Broadbent,  Sansom,  Byrom  Bramwell,  Gibson,  and  Allbutt. 

I  am  especially  indebted  to  the  masterly  article  on 
"  Enlargement  of  the  Heart "  in  Keating' s  Encyclopcedia  of 
the  Diseases  of  Children,  written  by  Dr.  Mitchell  Bruce, 
whose  nomenclature  with  respect  to  the  mode  of  production 
of  dilatation  of  the  heart  I  have  adopted  throughout  the 
book. 

The  illustrations  are  for  the  most  part  original,  but  I 
have  to  acknowledge  the  kindness  of  Messrs.  Charles  Griffin 
and  Co.,  and  Messrs.  Longmans,  Green,  and  Co.  in  permitting 
me  to  make  use  of  electrotypes  of  illustrations  appearing  in 
works  published  by  them. 

My  thanks  are  due  to  Dr.  J.  G.  Emmanuel,  late  Resident 
Medical  Officer  at  the  Chest  Hospital,  Victoria  Park,  for  a 
large  number  of  the  pulse  tracings. 

Dr.  Hugh  Walsham  has  kindly  placed  at  my  disposal  the 
skiagram  of  the  chest,  which  appears  as  a  frontispiece. 

E.  H.  C. 

London,  yaw2/«rj/  nth,  1901. 


TABLE    OF   CONTENTS 


CHAPTER  I 
Anatomy  pagh 

Position  and  shape  of  Heart  and  Pericardium — Size  and  weight  of  the  Heart 
— Dimensions  of  the  Auricles  and  Ventricles — Relative  position  of  the 
Cardiac  Orifices  and  Valves — Relative  size  of  the  Orifices  of  the  Heart — 
Relation  of  the  Heart  and  its  Orifices  to  the  Sternum  and  Ribs       .         .       I 

CHAPTER   H 

Physiology 

Cardiac  Cycle — Time  relations  and  sequence  of  the  various  events  which 

comprise  Cardiac  Cycle — Cardiac   Impulse  —  Its  position  and   cause  — 

Sounds  of  the  Heart — Their  cause  and  duration — Nervous  Supply  of  the 

Heart       .  .  .  .  .  .  .         .       g 

CHAFFER   III 

Methods  of  Diagnosis 
Enumeration  of  Methods — Section  I.  Symptomatology — Section  II.  ^Etiology 
— Section  III.  The  Physical  Methods  of  Di-agtiosis — Sub-section  I.  In- 
spection ;  general ;  local — Sub-section  II.  Palpation ;  Prsecordium ;  great 
vessels ;  other  organs — Sub-section  III.  Percussion ;  Heart ;  Pericardium ; 
great  vessels ;  other  organs — Sub-section  IV.  Auscultation;  Heart  Sounds 
and  their  Modifications;  Adventitious  Sounds;  Vascular  Sounds     .         .     i6 

CHAPTER   IV 

The  Pulse 
Definition — Method  of  Production — Physical  Examination  of  Pulse — Inspec- 
tion— Palpation — Graphic     Record      or      Sphygmogram — Instrumental 
Determination  of  the  Blood  Pressure        .  .  .  .  -74 

CHAPTER  V 

The  Cardiograph 

Its  Sphere  of  Usefulness — The   Normal   Cardiogram — Cardiograms   of  the 

Chief  Valvular  Lesions      ....  .  .     94 

CHAPTER  VI 

Congenital  Affections  of  the  Heart  and  Great  Vessels 

.(Etiology  and    Pathology  —  Classification  —  Symptoms  —  Physical    Signs — 

Diagnosis — Prognosis — Treatment  .  *  .  .  •99 


xii  TABLE   OF   CONTENTS 

CHAPTER  VII 
Diseases  of  the  Pericardium  page 

Classification — Section  I.  Acute  Pericarditis — Section  II.  Pericardial  Adhe- 
sion— Section  III.  Hydropericardium — Section  IV.  Haemopericardium 
— Section  V.  Pneumopericardium — Section  VI.   New  Growths        .         .116 

CHAPTER  VIII 

Acute  Endocarditis 
Classification — Section  I.  Acute  Simple  Endocarditis — Section  II.  Malignant 
or  Infective  Endocarditis         .  .  .  ...    138 

CHAPTER   IX 

Chronic  Endocarditis 
Pathogenesis — Morbid  Anatomy — Effects  on  the  Functions  of  the  Valves — 
Effects  on  the  Heart  and  Circulation — Effects  on  other  organs  .         .   160 

CHAPTER  X 

Chronic  Valvular  Lesions 
Pathogenesis  of  Chronic  Valvular  Disease  .  .  «  ,         .    165 

CHAPTER  XI 

Mitral  Incompetence 
Pathogenesis — Morbid  Anatomy — Compensation  :  its  method  of  production 
and  maintenance — Failure  of  Compensation,  and  its  results — Symptoms — 
Complications — Physical  Signs — Diagnosis — Estimation  of  the  amount  of 
Regurgitation  .  .  .  .  .  .         .   167 

CHAPTER  XII 

Mitral  Stenosis 
Pathogenesis — Morbid  Anatomy — Pathological  Effects  on  the  Heart  and 
Circulation  —  Symptoms — Complications  — Physical  Signs  — Diagnosis  — 
Estimation  of  the  degree  of  Stenosis     .  .  .  .         .   181 

CHAPTER  XIII 

Aortic  Incompetence 
Pathogenesis — Morbid  Anatomy  —  Effects  on  the  Heart  and  Circulation — 
Compensation—  Sudden    Death — Symptoms — Complications — Physical 
Signs — Diagnosis — Estimation  of  the  amount  of  Regurgitation    .  -195 

CHAPTER  XIV 

Aortic  Stenosis 
Pathogenesis — Morbid  Anatomy— Effects  on  the  Heart  and  Circulation  — 
Compensation  :    its  duration  and  failure — Symptoms — Complications— 
Mode  of  Termination — Physical  Signs — Diagnosis — Estimation  of  degree 
of  Stenosis  .  .  .  .  ...  207 


TABLE   OF   CONTENTS  xiii 

CHAPTER  XV 

Tricuspid  Incompetence  page 

Pathogenesis — Morbid  Anatomy — Effects  on  the  Heart  and  Circulation — 
Symptoms — Physical  Signs — Diagnosis — Estimation  of  the  amount  of 
Regurgitation  .  .  .  .  .  .        .  212 

CHAPTER  XVI 
Tricuspid  Stenosis 
Pathogenesis  —  Morbid  Anatomy — Effects  on  the  Heart  and  Circulation — 
Symptoms — Physical  Signs — Diagnosis — Estimation  of  degree  of  Stenosis  217 

CHAPTER  XVII 

Pulmonary  Incompetence 
Pathogenesis — Morbid  Anatomy — Effects  on  the  Heart  and  Circulation  — 
Association  with  other  Cardiac  Developmental  Anomalies — Symptoms — 
Physical  Signs — Diagnosis — Estimation  of  the  amount  of  Regurgitation  .   221 

CHAPTER  XVIII 

Pulmonary  Stenosis 
Pathogenesis — Morbid  Anatomy — Effects  on  the  Heart  and  Circulation — 
Symptoms — Physical   Signs — Diagnosis — Estimation  of  the  degree  of 
Stenosis  .  .  .  .  ...  225 

CHAPTER  XIX 
Combined  Valvular  Disease  .  .  ...  229 

CHAPTER  XX 
Prognosis  of  Chronic  Valvular  Disease        .  ...  230 

CHAPTER  XXI 
The  Treatment  of  Chronic  Valvular  Disease 
Prophylaxis — Treatment  before  Failure  of  Compensation — Treatment  after 
Failure  of  Compensation — Removal  of  Cause — Treatment  of  Effects — 
Use  of  Cardiac  Stimulants  and  Tonics  .  ...  234 

CHAPTER  XXII 

Diseases  of  the  Myocardium 
Classification — Section  I.  Hypertrophy  and  Dilatation  of  the  Heart ;  Defini- 
tion ;  Classification  of  Kinds  of  Cardiac  Enlargement ;  Morbid  Anatomy ; 
Effects  on  other  Organs ;  Pathogenesis ;  ^Etiology ;  Symptoms ;  Physical 
Signs;  Diagnosis;  Prognosis;  Treatment — Section  II.  Acute  Myocarditis ; 
^Etiology ;  Morbid  Anatomy ;  Effects  on  the  Heart ;  Symptoms ;  Physical 
Signs;  Diagnosis;  Prognosis;  Treatment — Section  HI.  Degenerative 
Diseases  of  the  Myocardium;  Definition;  iEtiology;  Morbid  Anatomy; 
Pathogenesis ;  Symptoms ;  Physical  Signs ;  Diagnosis ;  Prognosis ;  Treat- 
ment—  Section  IV.  Fatty  Diseases  of  the  Heart ;  Fatty  Infiltration ; 
Fatty  Degeneration — Section  V.  Fibroid  Disease  of  the  Heart — Section 
VI.  Growths  in  the  Heart      .  .  .  ...  248 


xiv  TABLE   OF   CONTENTS 

CHAPTER  XXIII 

Angina  Pectoris  page 

Etiology — Kinds  of  Angina — Morbid  Anatomy — Pathogenesis — Symptonas 
—Physical  Signs — Diagnosis — Prognosis  —Treatment  .  .         .  310 

CHAPTER  XXIV 

Functional  Disorders  of  the  Heart 
Definition — Etiology — Pathogenesis — Section  I.  Cardiac  Pain  ;  Local  and 
Referred — Section  II.  Palpitation  ;  Definition  ;  Causation  ;  Features  of 
Paroxysm  —  Section  III.  Cardiac  Asthenia  —  Section  IV.  Alterations  in 
the  Rhythm  of  the  Heart's  Action  ;  Arrhythmia  ;  Intermittence  and  Ir- 
regularity—  Section  V.  Alterations  in  the  rate  of  the  Heart's  Action — 
Section  VI.  Tachycardia  —  Section  VII.  Decrease  in  the  rate  of  the 
Heart's  Action — Section  VIII.    Diagnosis;   Prognosis;   Treatment       .  322 


Index  »  >  j  •  ■.  >  •        .  345 


LIST   OF    ILLUSTRATIONS 


FIG. 

r 


Section  through  the  base  of  the  heart,  showing  the  relations  of  the 
cardiac  orifices  and  valves  .  .  .  . 

Relation  of  the  heart  and  aorta  to  the  ribs  and  sternum    . 

The  position  of  the  valvular  orifices,  and  their  relation  to  the  cardiac 
dulness  .  .  .  .  .  , 

4.  Diagrammatic  representation  of  the  cardiac  cycle  ^ 

5.  Normal  Cardiogram  (Sansom  after  Galabin) 

6.  Diagrammatic  represeiUation  of  the  cardiac  sounds  with  reference  to 

the  cardiac  cycle  .  .  .  .  , 

7-    Diagrammatic  representation  of  the  diagnosis    . 

8.  The  areas  in  which  the  sounds  produced  at  the  various  cardiac  orifices 

are  most  distinctly  heard  .  .  .  . 

9.  Diagrammatic  representation  of  a  systolic  murmur 

10.  Diagrammatic  representation  of  an  entire  diastolic  murmur 

11.  Diagrammatic  representation  of  a  presystolic  murmur 

12.  Diagrammatic  representation  of  an  early  diastolic  murmur 

13.  Diagrammatic  representation  of  a  mid-diastolic  murmur  . 

14.  Normal  pulse  tracing  .  .  ,  .  '  . 

15.  Mahomed's  scheme  of  the  tidal  wave  .  .  . 

16.  High-tension  pulse  tracing  .  .  .  . 

17.  Low-tension  pulse  tracing  .  .  ,  . 

18.  Dicrotic  pulse  tracing  .  .... 

19.  Virtual-tension  pulse  tracing  ,  .  ,  .  ■ 

20.  Pulse  tracing  from  a  case  of  dilatation  of  the  heart  showing  respiratory 

curves  ...... 

21.  Pulse  tracing  from  a  case  of  aortic  regurgitation 

22.  Pulse  tracing  from  a  case  of  aortic  stenosis 

23.  Anacrotic  pulse  tracing        .  .  .  ,  . 

24.  Pulsus  Bisferiens  .  .... 

25.  Pulse  tracing  from  a  case  of  mitral  regurgitation 

26.  Pulse  tracing  from  a  case  of  mitral  stenosis 

27.  Pulse  tracing  taken  from  the  left  radial  artery  in  a  case  of  aneurism 

XV 


3 

5 

7 
10 
12 

13 
17 

44 
S6 
57 
57 
57 
57 
81 

83 
85 
86 
86 

87 


89 
90 
90 
90 
91 
91 
92 


xvi  LIST   OF  ILLUSTRATIONS 

FIG.  PAGE 

28.  Pulse  tracing  taken  from  the  right  radial  artery  in  the  same  case  (Fig.  27)  93 

29.  Normal  cardiogram  (Sansom  after  Galabin)        .                 .             .         .  94 

30.  Cardiogram  from  a  case  of  mitral  stenosis  (Sansom)          .             .         .  96 

31.  Cardiogram  from  a  case  of  mitral  stenosis  (Sansom)          .             .         .  97 

32.  Cardiogram  from  a  case  of  mitral  stenosis  (Sansom  after  Galabin)  97 

33.  Cardiogram  from  a  case  of  mitral  regurgitation  (Sansom)               .         .  97 

34.  Cardiogram  from  a  case  of  aortic  obstruction  (Sansom  after  Galabin)    .  98 

35.  Cardiogram  and  sphygmogram  from  a  case  of  aortic  regurgitation 

(Sansom)      .                .                .                .                ...  98 

36.  The  aortic  arches,   showing  mode  of    transformation  into  permanent 

arterial  trunks  (after  MacAlister,  modified)                 .             .         .  lOl 

37.  Diagrammatic  outline  of  the  organs  of  circulation  in  the  foetus  of  six 

months  (Thompson)     .                 .                 .                 ...  103 

38.  Diagrammatic  representation  of  an  entire  diastolic  murmur           .         .  189 

39.  Diagrammatic  representation  ol  a  presystolic  murmur       .             .         .  189 

40.  Diagrammatic  representation  of  an  early  aiastolic  murmur            -         .  189 

41.  Diagrammatic  representation  of  a  mid-diastolic  murmur                .         .  189 

42.  Bigeminal  pulse  tracing       .                 .                 .                 ...  332 

43.  Trigeminal  pulse  tracing     ,                ,                »                »            «         .  332 


DISEASES   OF  THE   HEART 


CHAPTER  I 
ANATOMY 


Position  and  shape  of  Heart  and  Pericardium^Size  and  weight  of  the  Heart — 
Dimensions  of  the  Auricles  and  Ventricles — Relative  position  of  the  Cardiac 
Orifices  and  Valves — Relative  size  of  the  Orifices  of  the  Heart — Relation  of 
the  Heart  and  its  Orifices  to  the  Sternum  and  Ribs 


The  heart  is  situated  in  that  portion  of  the  cavity  of  the  chest 
which  is  known  as  the  middle  mediastinum. 

The  Pericardium  :  its  shape  and  connections, — The  pericardium, 
wherein  the  heart  is  contained,  is  a  cone-shaped  membranous 
sac,  which  is  attached  by  its  base  to  the  middle  leaflet  of  the 
tendon  of  the  diaphragm,  and  by  its  apex  is  continuous  with  the 
fibrous  sheaths  of  the  great  vessels,  and  through  them  with  the 
cervical  fascia.  This,  the  outer  or  fibrous  layer  of  the  pericardium, 
is  lined  by  a  serous  coat,  which  is  reflected  along  the  great  vessels 
on  to  the  surface  of  the  heart,  and  completely  envelops  the  whole 
viscus.  The  space  between  the  two  layers  of  the  serous  covering 
is  known  as  the  cavity  of  the  pericardium.  Under  normal  conditions 
this  space  is  potential  rather  than  real,  since  the  two  layers  of  the 
sac  are  in  close  apposition. 

The  general  shape  of  the  heart  is  that  of  a  blunt,  flattened  cone, 
the  anterior  convex  surface  of  which  faces  upwards  and  forwards, 
while  the  more  flattened  posterior  looks  downwards  and  backwards. 

The  shape  and  position  of  the  h;art. — The  base  of  the  organ 
is  directed  upwards,  backwards,  and  to  the  right,  extending  from 
the  level  of  the  sixth  to  the  eighth  dorsal  vertebra,  and  the  apex 
points  downwards,  forwards,  and  to  the  left.  During  life  the 
apex  beat  is  palpable  in  the  space  between  the  cartilages  of  the  fifth 

B 


2  DISEASES    OF   THE    HEART 

and  sixth  ribs,  about  3-|-  inches,  or  9  cm.,  from  the  mid-sternal  line. 
In  the  child  the  apex  beat  is  situated  in  the  fourth  interspace. 

Of  the  two  borders  of  the  heart,  which  are  formed  by  the 
junction  of  the  anterior  and  posterior  surfaces,  the  one  {inargo 
acutus),  longer  and  thinner,  looks  forwards  and  downwards,  while 
the  other  {inargo  obtusus),  shorter  and  more  rounded,  is  directed 
backwards  and  to  the  left. 

The  axis  of  the  heart  is  inclined  to  the  horizon  at  an  angle  of 
40°,  and  the  greater  portion  of  the  organ  is  situated  to  the  left  of 
the  median  line. 

The  position  of  the  heart  is  affected  to  some  extent  by  posture, 
and  by  the  degree  of  distension  of  the  lungs.  Except  at  its  base, 
where  it  is  attached  to  the  great  vascular  trunks,  the  heart  lies 
entirely  free  within  the  pericardial  sac. 

It  will  be  observed  that  although  the  pericardium  and  heart  are 
both  conical  in  shape,  the  bases  of  the  two  cones  do  not  coincide. 
Thus  in  the  case  of  the  pericardium  the  base  of  the  cone  looks 
downwards,  while  in  that  of  the  heart  it  is  directed  upwards,  back- 
wards, and  to  the  right. 

The  relations  of  the  heart. — The  anterior  surface  of  the  heart 
is  completely  overlapped  by  the  pleurae  and  lungs,  except  over  its 
lower  part,  where  a  roughly  triangular  area,  to  the  left  of  the  median 
line,  remains  uncovered.  This  uncovered  portion  of  the  wall  of  the 
heart,  which  corresponds  with  the  area  of  superficial  cardiac  dul- 
ness,  will  be  more  accurately  defined  in  a  subsequent  paragraph. 

The  size  and  weight  of  the  organ,  — The  size  and  weight  of 
the  heart  are  liable  to  considerable  variation,  in  accordance  with  the 
age,  sex,  stature,  and  muscular  development  of  the  subject,  as  well 
as  with  the  method  of  removal  that  is  adopted.  The  following 
figures,  therefore,  must  be  looked  upon  as  representing  average 
measurements  only. 

The  weight  of  the  adult  male  heart  averages  1 1  ounces,  or  about 
310  grammes;  the  weight  of  the  adult  female  heart  9  ounces,  or 
about  255  grammes.  As  a  general  rule,  the  adult  has  about 
5  grammes  of  heart  weight  for  each  kilo  of  body  weight ;  or,  stated 
more  exactly,  the  proportion  of  heart  weight  to  body  weight  in  the 
male  is  as  i  to  178,  and  in  the  female  as  i  to  169  (Macalister). 

External  markings. — The  external  surface  of  the  heart  is  divided 
into  auricular  and  ventricular  portions  by  a  deep  transverse  groove 
— the  auriculo-ventricular  furrow.  The  division  between  the  ven- 
tricles is  shown  by  two  shallow  interventricular  grooves,  which, 
running  from  and  at  right  angles  to  the  auriculo-ventricular  furrow, 
become  continuous  with  one  another  a  little  to  the  right  of  the  apex. 
It  will  thus  be  seen  that  the  apex  of  the  heart  is  formed  entirely  by 
the  left  ventricle.     Moreover,  owing  to  the  position  of  the  organ, 


ANATOMY  3 

the  right  ventricle  forms  the  greater  portion  of  the  anterior  surface 
of  the  heart,  and  the  left  of  the  posterior. 

Size  and  dimensions  of  tlie  heart. — The  capacity  of  each  of  the 
four  cavities  of  which  the  heart  is  composed  is  approximately  the 
same,  and  may  be  put  at  loo  cc,  or  about  3I-  ounces. 

The  walls  of  the  different  chambers  vary  greatly  in  thickness.    The 


'/       /-■A 


T 


M 


IG.    I.      SECTION   THROUGH   THE   EASE   OF   THE   HEART,    SHOWING   THE 

RELATIONS   OF   THE   CARDIAC    ORIFICES   AND   VALVES 

P= pulmonary  orifice;  A= aortic  orifice  ;  M  =  mitral  opening  ;  T  =  tricuspid  opening 


average  thickness  of  the  auricular  walls  is  about  i  mm.,  or  J^  of 
an  inch.  The  wall  of  the  left  auricle  has  a  maximum  thickness  of 
3  mm.,  or  \  of  an  inch,  and  the  wall  of  the  right  auricle  2*5  mm., 
or  y\j-  of  an  inch.  The  thickness  of  the  wall  of  the  left  ventricle 
ranges  between  4  mm.  and  i  cm.  (p  to  h,  inch),  and  of  the  right 
ventricle  between  2  mm.  and  4  mm.  \~^  to  \  inch). 


4  DISEASES   OF   THE   HEART 

Relative   position    of   the   cardiac    orifices    and   valves. — The 

relative  position  of  the  various  orifices  with  their  valves  is  most 
readily  appreciated  by  means  of  a  transverse  section  taken  just  above 
the  ventricles,  so  that  the  structures  exposed  can  be  viewed  from 
above. 

The  accompanying  diagram  illustrates  such  a  section  (Fig.  i). 

Pulmonic  orifice. — It  will  be  observed  that  the  conus  arteriosus 
crosses  the  aortic  opening  obliquely  from  right  to  left,  whence  it 
happens  that  the  pulmonic  orifice  is  carried  in  front  of  and  slightly 
to  the  left  of  the  aortic. 

Aortic  orifice. — The  orifice  of  the  aorta  lies  in  front  of  and 
between  the  two  auriculo-ventricular  openings. 

The  aortic  and  pulmonic  orifices  are  each  guarded  by  a  valve  con- 
sisting of  three  semilunar  flaps,  which  are  differently  arranged  at  the 
two  openings. 

At  the  aortic  orifice  one  flap  is  anterior  and  to  the  right,  one 
anterior  and  to  the  left,  and  the  other  posterior  and  to  the  right ; 
while  at  the  pulmonic  opening  one  is  anterior  and  to  the  left,  one 
posterior  and  to  the  left,  and  the  third  posterior  and  to  the  right. 

Mitral  opening. — The  left  auriculo-ventricular  or  mitral  orifice 
is  situated  immediately  behind  and  to  the  left  of  the  aortic  opening. 
It  is  guarded  by  a  valve  composed  of  a  small  posterior  and  a  larger 
anterior  curtain,  the  latter  of  which  separates  the  mitral  from  the 
aortic  orifice.  The  close  proximity  of  the  large  anterior  flap  of  the 
mitral  valve  to  the  orifice  of  the  aorta  is  of  some  clinical  importance, 
and  will  be  again  referred  to. 

Tricuspid  opening. — The  right  auriculo-ventricular  or  tricuspid 
opening  is  closed  by  a  valve  consisting  of  three  segments,  of  which 
one  is  placed  anterior  and  to  the  left,  a  second  to  the  right,  and  the 
third  posteriorly. 

It  is  worthy  of  notice  that  the  dimensions  of  the  aortic  and  pul- 
monic orifices  are  anatomically  incapable  of  any  alteration  at  the 
time  of  the  closure  of  the  semilunar  valves.  On  the  other  hand, 
the  size  of  the  auriculo-ventricular  openings  is  very  much  diminished 
during  systole,  in  order  to  enable  the  valvular  curtains  to  come  into 
accurate  apposition.  This  difference  in  the  mechanism  of  closure 
of  the  two  sets  of  openings  has,  as  will  be  seen,  important  patho- 
logical and  clinical  bearings. 

The  following  measurements  (taken  from  Macalister's  Text  Book 
of  Human  Anatoniy)  are  of  some  interest  as  showing  the  relative  size 
of  the  orifices  of  the  heart : — • 

Area  of  the  tricuspid  orifice  in  sq.  mm. 
Area  of  the  mitral  orifice  „ 

Area  of  the  aortic  opening  „ 

Area  of  the  pulmonic  opening     „ 


xMales. 

Females. 

I27"0 

..        105-0 

96'o 

..        86-8 

7o"6 

65*2 

68-5      . 

••        64-5 

ANATOMY 


5 


Topography  of  the  heart. — It  has  already  been  mentioned  that 
nearly  two-thirds  of  the  bulk  of  the  heart  lie  to  the  left  of  the 
median  line  of  the  body.  The  upward  extent  of  the  organ  is  repre- 
sented on  the  surface  of  the  chest  by  a  horizontal  line  drawn  slightly 
below  the  level  of  the  second  costal  cartilages.  The  heart  hes  to 
the  left  of  a  vertical  line  drawn  downwards  from  the  sternal  end 


FIG.    2,    RELATION    OF   THE    HEART   AND    AORTA   TO  THE    RIBS    AND    STERNUM 

L.V.  =  left  ventricle  ;  R.V.=right  ventricle;  L.A.  =  left  auricle  ;  R.A.  =  right  auricle  ; 
A.=aorta;  P.A.  =  pulmonary  artery  ;  V.  C.  =  vena  cava. 

of  the  right  clavicle,  and  to  the  right  of  an  oblique  line  considerably 
convex  upwards  and  outwards,  drawn  from  the  second  costal  carti- 
lage about  an  inch  from  the  left  sternal  border  to  the  upper  border 
of  the  sixth  costal  cartilage,  9  cm.  or  3^^  inches  from  the  mid-sternal 
line.  It  lies  above  a  line,  very  slightly  concave  upwards,  drawn  from 
the  upper  border  of  the  sixth  rib,  9  cm.  from  the  mid-sternal  line,  to 
the  lower  border  of  the  cartilage  of  the  right  fifth  rib,  close  to  the 
sternal  edge. 

The  width  of  the  heart  at  the  level  of  the  fourth  costal  cartilage  is 
about  4^  inches,  of  which  i|-  inches  lie  to  the  right  of  the  mid- 
sternal  line,  and^  3  inches  (nearly)  to  the  left. 


6  DISEASES   OF   THE    HEART 

Area  of  deep  cardiac  dulness. — The  whole  of  this  area  marks 
out  what  is  known  as  the  region  of  "  deep  cardiac  dulness,"  and 
corresponds  approximately  with  the  absolute  size  of  the  heart  so  far 
as  its  anterior  aspect  is  concerned. 

Area  of  superficial  cardiac  dulness. — By  the  term  superficial 
cardiac  dulness  is  meant  the  extent  of  the  cardiac  surface  un- 
covered by  the  margins  of  the  lungs,  and  in  contact,  through  the 
pericardium,  with  the  chest  wall.  This  area  is  included  in  a  triangle, 
which  is  bounded  by  the  mid-sternal  line,  by  a  line  drawn  from  a 
point  on  the  mid-sternal  line,  opposite  the  level  of  the  upper  border 
of  the  fourth  costal  cartilages,  to  the  lower  border  of  the  fifth  left 
costal  cartilage,  at  its  junction  with  the  rib,  and  by  a  line  drawn  hori- 
zontally inwards  from  this  point  to  the  mid-sternal  line. 
For  practical  purposes  the  area  of  superficial  cardiac  dulness  may 

also  be  defined  by  a  circle  2  inches  in  diameter,  drawn  from  a  point 

midway   between   the   left   nipple   and   the   end   of    the    gladiolus 

(Latham). 

The  relation  of  the  different  chambers  and  orifices  of  the  heart 

to  the  area  of  deep  cardiac  dulness  will  now  be  described. 

Right  auricle. — The  right  auricle  lies  behind  the  sternal  end.s 
(about  I J  inches  from  the  mid-sternal  line)  of  the  third,  fourth,  and 
fifth  costal  cartilages,  the  second,  third,  and  fourth  intercostal  spaces, 
and  the  right  sternal  edge.  The  apex  of  the  right  auricular  appendix 
is  situated  in  the  middle  line  opposite  the  level  of  the  upper  border 
of  the  third  costal  cartilages. 

Left  auricle. — The  only  part  of  the  left  auricle  that  is  visible 
from  the  front  is  its  appendix,  which  is  placed  behind  the  second 
left  interspace  and  upper  part  of  the  third  costal  cartilage  about 
i|-  inches  from  the  left  sternal  edge. 

Eight  ventricle. — The  greater  portion  of  the  anterior  surface 
of  the  heart  consists  of  the  wall  of  the  right  ventricle,  which, 
measured  along  the  left  edge  of  the  sternum,  extends  from  just 
above  the  third  rib  to  the  lower  border  of  the  sixth  costal  cartilage. 
Its  upper  part  is  formed  by  the  conus  arteriosus,  and  is  uncovered 
by  lung. 

Left  ventricle. — The  left  ventricle  forms  the  left  border  of  the 
heart  as  high  as  the  upper  border  of  the  third  rib,  and  also  the  apex 
of  the  organ.  The  apex  of  the  heart  in  adults  is  situated  in  the 
fifth  intercostal  space,  9  cm.  or  3J  inches  from  the  mid-sternal  line. 

A  diagrammatic  representation  of  these  relations  is  shown  in  the 
preceding  figure. 

Tricuspid  opening.— The  right  auriculo-ventricular  or  tricuspid 
opening  is  behind  the  middle  of  the  sternum  opposite  the  fourth 
costal  cartilages. 


ANATOMY  7 

Mitral  opening. — The  left  auriculo-ventricular  or  mitral  orifice 
lies  behind  the  sternum,  to  the  left  of  the  middle  line,  on  a  level 
with  the  upper  border  of  the  fourth  costal  cartilages. 

Aortic  orifice. — The  aortic  opening  is  situated  behind  the 
sternum  to  the  left  of  the  middle  Hne  on  a  level  with  the  lower 
border  of  the  third  costal  cartilages.  The  ascending  portion  of  the 
aorta  extends  from  this  point  to  the  level  of  the  upper  border  of 
the  second  right  costal  cartilage  at  its  junction  with  the  sternum. 

Pulmonic  orifice. — The  pulmonic  orifice  lies  behind  the  upper 
border  of  the  third   left   costal   cartilage  at  its   junction   with  the 


FIG.    3.       THE    POSITION    OF    THE   VALVULAR   ORIFICES,    AND   THEIR    RELATION 
TO   THE   CARDIAC    DULNESS 

P = pulmonary  orifice  ;  A  =  aortic  orifice  ;  M  =  mitral  orifice  ;  T  =  lricuspid  orifice 
P  (within  circle) = pulmonary  area  ;  A  (within  circle) = aortic  area 
M  (within  circle)=mitral  area  ;  T  (within  circle)  =  tricuspid  area 


Sternum.     The  vessel  ascends  vertically  from  this  point  to  the  level 
of  the  second  left  costal  cartilage,  behind  which  it  bifurcates. 

The  auriculo-ventricular  sulcus. — The  auriculo-ventricular  sulcus 
is   represented   by   a   line   drawn    from    the   upper  border   of  the 


8  DISEASES  OF  THE  HEART 

cartilage  of  the  sixth  rib  on  the  right  side,  at  its  junction  with 
the  sternum,  to  the  upper  edge  of  the  third  left  costal  cartilage 
close  to  the  sternal  border. 

The  interventricular  sulcus. — The  anterior  interventricular  groove 
corresponds  with  an  oblique  line,  slightly  concave  inwards,  drawn 
from  a  point  half  an  inch  inside  the  apex,  to  the  upper  border  of  the 
third  left  costal  cartilage,  i^  inches  from  the  left  sternal  edge. 

It  must  be  borne  in  mind  that  the  foregoing  landmarks  are  subject 
to  considerable  variation  in  different  individuals,  according  to  age, 
muscular  and  bony  development,  etc.  In  children  the  apex  of  the 
heart  is  situated  a  space  higher  than  in  adults,  i.e..  in  the  fourth 
intercostal  space,  and  further  to  the  left,  so  that  it  is  often  found  in  the 
nipple  line,  or  even  slightly  outside  this  limit. 

Aorta. — The  first  or  ascending  portion  of  the  aortic  arch  extends 
from  the  lower  border  of  the  third  left  costal  cartilage  to  the  upper 
border  of  the  second  right  costal  cartilage  at  its  junction  with  the 
sternum.  The  transverse  portion  of  the  arch  runs  across  the  sternum 
below  the  level  of  a  line  drawn  horizontally  through  the  middle  of  the 
manubrium,  to  the  upper  border  of  the  fourth  dorsal  vertebra. 

The  third  or  descending  portion  of  the  arch  lies  to  the  left  of  the 
body  of  the  fourth  dorsal  vertebra. 


CHAPTER   II 
PHYSIOLOGY 


Cardiac  Cycle — Time  relations  and  sequence  of  the  various  events  which  com- 
prise Cardiac  Cycle — Cardiac  Impulse — Its  position  and  cause — Sounds  of 
the  Heart — Their  cause  and  duration — Nervous  Supply  of  the  Heart 

The  term  cardiac  cycle  is  applied  to  that  sequence  of  events 
which  is  included  in  each  successive  beat  of  the  heart.  It  is  com- 
posed of  a  contraction  or  systole  of  the  auricles,  a  contraction  or 
systole  of  the  ventricles,  and  a  pause  or  period  during  which  all 
four  chambers  of  the  heart  undergo  relaxation,  and  then  remain  in 
a  state  of  passivity  {i.e.  a  condition  in  which  the  muscular  walls 
neither  contract  nor  relax)  until  the  commencement  of  the  succeed- 
ing cardiac  cycle.     This  pause  is  called  diastole. 

The  phases  of  contraction  and  relaxation  on  the  right  and  left 
sides  of  the  heart  are,  under  normal  conditions,  exactly  synchronous 
in  the  corresponding  chambers. 

The  normal  rate  of  the  heart's  action  may  be  taken  to  be  seventy- 
five  beats  per  minute,  so  that  each  complete  cardiac  cycle  is  about 
eight-tenths  (y^^)  o^  ^  second  in  duration.  The  times  occupied  by 
the  individual  phases  are  approxi?jiately  as  follows  : — 

Auricles.         Ventricles 


Systole  of  the  auricles 
Systole  of  the  ventricles 
Diastole  of  the  auricles  : 

Relaxation 

Passive  interval 
Diastole  of  the  ventricles 

Relaxation 

Passive  Interval    . 
Total  Cardiac  Cycle 


1 0  sec. 
TTT  sec 


sec. 


sec. 


sec. 


It  must  be  clearly  understood  that  the  clinical  uses  of  the  terms 
"systole"  and  "diastole"  apply  solely  to  these  conditions  in  the 
ventricles.  Consequently  "  systole,"  as  applied  to  the  phases  of 
the  cardiac  cycle,  includes  the  ventricular  contraction,  and  part  of 

9 


JO 


DISEASES    OF   THE    HEART 


the  auricular  relaxation ;  while  "diastole"  comprises  the  ventricular 
relaxation,  part  of  the  auricular  relaxation ;  the  passive  interval,  and 
the  whole  of  the  auricular  contraction  (see  diagram  Fig.  4). 


■eSecs. 


■^Secs. 

FIG.    4.       DIAGRAMMATIC    REPRESENTATION    OF   THE   CARDIAC   CYCLE 


By  the  successive  contractions  of  the  auricles  and  ventricles  the 
blood  passes  from  the  former  into  the  latter,  and  from  the  latter 
into  the  arterial  trunks.  A  reflux  is  prevented  by  the  interposition 
of  valves  between  the  auricles  and  ventricles,  and  at  the  orifices 
of  the  aorta  and  pulmonary  artery.  The  flaps  of  these  valves  come 
together  and  close  the  openings  which  they  guard  so  soon  as  the 
blood  pressure  in  front  of  them  becomes  greater  than  in  the  chamber 
immediately  behind  them.  There  is  no  valvular  mechanism  to 
prevent  a  reflux  of  blood  from  the  auricles  into  the  large  veins 
during  the  auricular  contraction,  but  immediately  before  and  during 
the  auricular  systole  there  is  a  similar  contraction  of  the  muscular 
walls  of  those  portions  of  the  large  veins  which  lie  nearest  the  heart, 
and  a  consequent  narrowing  of  their  lumen,  so  that  the  blood  takes 
the  path  of  least  resistance,  and  passes  through  the  auriculo- 
ventricular  openings  into  the  ventricles. 


PHYSIOLOGY  II 

Blood  passes  into  the  ventricles  during  the  whole  of  the  ventricular 
diastole  largely  in  consequence  of  the  positive  pressure  which 
prevails  in  the  veins  and  auricles,  but  in  some  measure,  no  doubt, 
owing  to  the  negative  pressure  which  obtains  in  the  ventricular 
chambers,  by  reason  of  the  active  dilatation  of  their  walls.  The 
final  process  of  filling  the  ventricles  is  completed  by  the  auricular 
systole. 

The  time  relations  and  sequence  of  the  various  events  which 
comprise  the  cardiac  cycle  are  illustrated  by  the  preceding  diagram. 
The  outer  and  inner  circles  represent  the  movements  of  the 
auricles  and  ventricles  respectively.  The  radial  and  circular  lines 
between  the  circles  represent  the  contraction  and  relaxation  of 
the  auricles  and  ventricles  respectively.  The  passive  interval 
is  left  blank,  while  each  eighth  part  of  the  circumference  of 
the  circles  represents  one-tenth  of  a  second.  The  most  constant 
feature  of  the  cardiac  cycle,  with  different  rates  of  heart  beat, 
is  the  duration  of  the  ventricular  systole.  Hence  it  follows  that 
an  increase  in  the  rate  of  the  heart's  action  is  obtained  chiefly  by 
means  of  the  shortening  of  the  diastole. 

The  cardiac  impulse. — The  cardiac  impulse  is  the  visible  and 
palpable  pulsation  of  the  heart  against  the  chest  wall.  It  is  syn- 
chronous with  the  systole  of  the  ventricles,  and  can  be  most 
distinctly  seen  and  felt  in  the  fifth  left  intercostal  space,  about  half 
to  one  inch  on  the  sternal  side  of  the  vertical  nipple  line.  The  site 
and  force  of  the  cardiac  impulse  vary  somewhat  with  the  position  of 
the  body. 

The  cause  of  the  cardiac  impulse  is  briefly  as  follows.  In  the 
state  of  rest,  during  diastole,  the  heart  lies  with  its  axis  directed 
obliquely  downwards,  so  that  the  apex  of  the  organ  (in  the  up- 
right position  at  all  events)  is  in  contact  with  the  chest  wall  at  the 
point  mentioned  above.  During  systole  the  heart,  besides  being 
tilted  slightly  upwards,  moves  forwards  and  to  the  right,  whereby  the 
apex  is  brought  into  closer  contact  with  the  thoracic  parietes  at  a 
time  when  the  wall  of  the  ventricles  suddenly  becomes  tense  and 
hard.  Furthermore,  the  antero-posterior  diameter  of  the  heart  is 
increased  during  systole,  and  in  this  way  the  anterior  surface  of  the 
ventricles  is  also  brought  nearer  to  the  chest  wall.  The  total  effect 
of  these  changes  is  to  bring  the  apex  and  adjacent  portion  of  the 
cardiac  wall,  during  systole,  into  somewhat  violent  contact  with  the 
thoracic  parietes  in  the  position  of  the  apex  beat. 

The  cardiac  impulse,  therefore,  is  the  local  displacement  of  the 
thoracic  parietes  produced  by  the  more  or  less  forcible  impact  of 
the  apex  and  adjacent  portion  of  the  hardened  and  rigid  cardiac 
wall  during  the  ventricular  systole. 

A  lengthening  of  the  long  axis  of  the  heart  is  not  concerned  in 
the  production  of  the  apex  beat,  inasmuch  as  this  diameter  of  the 
organ  remains  apparently  unaltered  during  systole  and  diastole. 

If  the  heart's  impulse  be  allowed  to  impinge  on  the  end  of  a 
lever,  or  on  the  membrane  of  a  tambour  in  one  of  the  manv  forms 


12  DISEASES    OF   THE    HEART 

of  cardiograph,  a  tracing  or  impulse  curve  may  be  obtained,  which 
will  be  considered  more  fully  later  (see  p.  94). 

The  following  is  a  normal  cardiogram  : — 


5.       NORMAL   CARDIOGRAM 
(Saiisom  afi'ar  Galabin) 


The  sounds  of  the  heart,  —  On  listening  over  the  region  of 
the  heart  two  sounds  may  be  distinguished,  which  have  been 
likened  to  the  pronunciation  of  the  syllables  lubb-dup.  The  first 
sound,  as  indicated  by  the  consonous  syllable  lubb,  is  comparatively 
dull,  deliberate,  and  prolonged  ;  while  the  second  sound,  represented 
by  diip,  is  sudden,  sharp,  and  short.  The  interval  between  the  first 
and  second  sounds  is  very  short,  while  that  between  the  second  and 
succeeding  first  sound  is  relatively  of  considerable  duration.  By 
direct  observation  it  has  been  proved  that  the  first  sound  is 
synchronous  with  the  ventricular  systole,  and  the  second  sound  with 
the  closure  of  the  semilunar  valves.  The  first  sound  of  the  heart 
is  caused  partly  by  the  tension  vibration  of  the  segments  of  the 
auriculo-ventricular  valves,  consequent  on  the  sudden  closure  of 
their  orifices ;  partly  by  the  so-called  muscular  sound,  which  is  pro- 
duced by  the  vibration  of  the  muscular  wall  of  the  ventricles, 
consequent  on  their  contraction ;  and  partly  by  the  vibration  of  the 
mass  of  blood  in  the  ventricles  and  of  the  chordai  tendine^. 

The  second  sound  is  due  partly  to  the  tension  vibration  of  the 
semilunar  cusps,  consequent  on  the  simultaneous  and  sudden  closure 
of  the  aortic  and  pulmonic  valves,  and  partly  to  the  vibration  of  the 
column  of  blood  in  the  aorta  and  pulmonary  artery. 

The  duration  of  the  cardiac  sounds,  and  more  especially  of  the 
pauses  between  them,  is  subject  to  considerable  variation,  but  the 
average  times  of  these  incidents,  and  their  relation  to  the  events 
comprising  the  cardiac  cycle,  are  represented  in  the  accompanying 
diagram.  (Fig.  6.) 

The  nerves  of  the  heart. — The  nervous  supply  of  the  heart  is 
derived  from  two  sources,  namely,  from  the  pneumogastric  or  vagi, 
and  sympathetic  nerves. 


PHYSIOLOGY 


13 


The  pneumogastric  branches  are  as  follow : — 

1.  The  superior  cardiac  branches,  two  or  three  in  number,  leave  the 

vagus  between  the  superior  and  inferior  laryngeal  branches. 

2.  The   inferior   cardiac    branches   arise   partly   from   the   superior 

laryngeal  nerve  and  partly  from   the   main  vagus  trunk  as  it 
enters  the  thorax. 

^      -8  Sees  ^ 


■CSecs.  I 


ZSecs. 


■4  Sees. 

FIG.    6.      DIAGRAMMATIC   REPRESENTATION   OF   THE   CARDIAC   SOUNDS 
WITH    REFERENCE   TO   THE    CARDIAC   CYCLE 

The  sympathetic  branches  are  as  follow  : — 

1.  The  superior  cardiac  branch  from  the  superior  cervical  ganglion. 

2.  The  middle  cardiac  branches  (composed  of  small  strands)  from 

the  middle  cervical  ganglion. 

3.  The  inferior  cardiac  branches  derived  from  several  small  strands 

from  the  inferior  cervical  and  first  dorsal  ganglia. 

Physiological  experiment  shows  that  in  the  dog,  and  presumably 
in  man,  the  sympathetic  fibres  leave  the  spinal  cord  by  the  anterior 
roots  of  the  second  and  third  dorsal  nerves,  and  then  pass  by 
the  rami  communicantes  to  the  ganglia  stellata  (ist  thoracic)  and 
thence  by  the  annulus  of  Vieussens  to  the  inferior  cervical  ganglia, 
whence  they  are  distributed  to  the  heart  via  the  cervical  ganglia. 


14  DISEASES    OF   THE    HEART 

All  three  branches  unite  in  the  cardiac  plexus,  which  may  be 
described  as  consisting  of  a  superficial  and  a  deep  portion.  The 
former  lies  in  front  of  the  arch  of  the  aorta  on  its  concave  border ; 
the  latter  lies  behind  the  aorta  at  a  higher  level  than  the  superficial 
portion  of  the  cardiac  plexus. 

From  these  two  plexuses  {i.e.  superficial  and  deep)  nerves  pass 
directly  to  supply  the  auricular  walls.  The  main  distribution,  how- 
ever, is  by  two  separate  strands  which  accompany  the  right  and  left 
coronary  arteries,  and  are  called  the  right  and  left  coronary  plexuses 
respectively.  The  right  coronary  plexus  supplies  chiefly  the  posterior 
surface  of  the  heart,  while  the  left  coronary  plexus  is  distributed 
mainly  over  the  left  ventricle. 

A  large  number  of  ganglion  cells  are  interpolated  along  the  course 
of  the  nerves  composing  these  plexuses,  more  especially  in  the  inter- 
ventricular and  auriculo-ventricular  grooves.  From  these  ganglion 
cells  a  large  number  of  fine  nerve  processes  penetrate  the  substance 
of  the  heart  to  be  distributed  to  the  individual  muscular  fibres,  as 
well  as  to  the  intermuscular,  sub-endocardial,  and  sub-pericardial 
tissues. 

The  nuclei  of  the  pneumogastric  nerves,  or  rather  those  parts  of 
them  which  supply  the  heart,  viz.  the  accessory  portions,  are  situated 
in  the  medulla  oblongata,  in  close  proximity  to  the  respiratory 
and  vaso-motor  centres. 

The  sympathetic  fibres  have  also  a  central  connection  with  cells 
in  the  medulla  and  upper  part  of  the  spinal  cord.  The  cells  con- 
nected with  the  sympathetic  fibres  do  not  appear,  however,  to  be 
aggregated  into  a  definite  centre,  but  seem  rather  to  be  distributed 
as  a  series  of  centres  through  the  upper  portion  of  the  spinal  cord, 
with,  probably,  a  controUing  centre  in  the  medulla,  situated  near  the 
pneumogastric  nucleus. 

The  regulation  of  the  beat  of  the  heart,  so  far  as  this  is  deter- 
mined by  nervous  influences,  is  effected  for  the  most  part,  if  not 
entirely,  either  directly  or  reflexly,  through  these  centres.  With 
regard  to  function  the  pneumogastric  centres  have  been  termed 
"  cardio-inhibitory,"  and  the  sympathetic  centres  "cardio-accelerator" 
or  "cardio-augmentor,"  inasmuch  as  those  impulses  which  diminish 
the  force  and  rate  of  the  heart's  action  and  prolong  diastole,  reach 
the  heart  by  way  of  the  pneumogastric  nerves ;  while  those  impulses 
which  increase  the  force  and  rate  of  the  heart's  action  and  shorten 
diastole  reach  the  organ  by  way  of  the  sympathetic  fibres. 

The  action  of  the  cardiac  centres  can  be  affected— 

1.  Directly,  by  the  condition  of  the  blood,  by  drugs,  by  altera- 

tions in  blood  pressure,  etc. 

2.  Reflexly,  by — 

(a)    Afferent  impulses  reaching  the  centres  from  the  heart. 


PHYSIOLOGY  15 

(P)  Afferent  impulses  from  other  organs,  notably  from  the 
abdominal  organs. 

(7)  Afferent  impulses  from  the  higher  nervous  centres  originat- 
ing in  emotion,  anxiety,  grief,  etc.,  or  sensory  impressions 
in  the  form  of  pain. 

(5)  Vaso-motor,  respiratory,  and  other  influences. 

It  must  be  borne  in  mind  that,  quite  apart  from  nervous  influences, 
the  cardiac  muscle  has  the  power  of  independent  rhythmical  con- 
traction; a  power  which  is,  however,  but  feebly  developed  in  the 
mammahan  heart.  Nevertheless  the  beat  of  the  heart  can  be,  and 
is,  profoundly  modified  by  influences  acting  directly  on  the  cardiac 
muscle,  and  possibly  on  the  cardiac  ganglia.  The  function  of  the 
cardiac  ganglia  is  not  fully  known,  but  their  influence  on  the  regula- 
tion or  modification  of  the  heart's  action  is  probably  quite  subsidiary. 

The  more  important  conditions  which  exert  a  direct  influence  on 
the  cardiac  muscle  and  thereby  modify  the  beat  of  the  heart  are  : — 

1.  Mechanical  stimuli. — The  heart  is  seldom  exposed  to  mechanical 

stimuli;  but  the  pressure  that  is  not  uncommonly  exerted 
on  the  organ  by  a  distended  stomach,  etc.,  may  be  classed 
under  this  head. 

2.  Alterations  in  the  quantity  and   quality  of  the  blood,   both 

physiological  and  pathological ;  drugs,  etc. 

3.  The  degree  of  distension   of  the   cardiac  chambers,   as,   for 

instance,  may  be  affected  by  respiration,  alterations  in  blood 
pressure,  or  by  disease  in  the  form  of  valvular  incompetence 
or  stenosis  of  an  orifice,  etc. 

Here  the  distension  of  one  or  other  of  the  cardiac  chambers 
increases  the  tension  of  its  walls,  and  by  this  means  gives  rise,  within 
certain  limits,  as  in  the  case  of  skeletal  muscle,  to  a  more  forcible 
contraction  of  the  heart. 


CHAPTER   III 
METHODS  OF  DIAGNOSIS 


Enumeration  of  Methods — Section  1.  Symptomatology — Section  II.  Etiology — 
Section  III.  The  Physical  Methods  of  Diagnosis — Sub-section  I.  Inspection  ; 
general ;  local — Sub-section  II.  Palpation  ;  Prsecordium  ;  great  vessels  ;  other 
organs — Sub-section  III.  Percussion  ;  Heart ;  Pericardium  ;  great  vessels  ; 
other  organs — Sub-section  IV.  Auscultation  ;  Heart  Sounds  and  their  Modifi- 
cations ;  Adventitious  Sounds  ;  Vascular  Sounds. 


The  diagnosis  in  cases  of  heart  disease  is  based  on — 

1.  The  symptoms. 

2.  The  causal  conditions  indicated  by  the  age,  sex,  occupation, 

and  history  of  the  patient. 

3.  The  physical  examination  of  the  patient,  which  consists  in  the 

use  of  certain  modes  of  procedure,  distinguished  under  the 
titles  of  Inspection,  Palpation,  Percussion,  and  Auscultation. 
These  physical  methods  of  diagnosis  should  always  be  em- 
ployed in  the  order  in  which  they  are  named. 

Each  element  in  the  diagnosis  will  now  be  considered  under  the 
headings  of  Symptomatology,  Etiology,  and  the  Physical  Methods 
of  Diagnosis.  A  short  account  of  the  pulse  and  of  the  clinical  uses 
of  the  sphygmograph  and  cardiograph  will  complete  the  chapter. 

SECTION    I 

SYMPTOMATOLOGY 

Disease  of  the  heart  may  exist  for  a  long  time  without  giving  rise 
to  symptoms  of  any  kind.  Thus  it  not  very  uncommonly  happens 
that  the  presence  of  a  cardiac  lesion  remains  unsuspected  until  some 
accidental  circumstance,  such  as  a  medical  examination  for  life 
insurance  or  for  one  of  the  public  services,  reveals  its  existence. 

The  symptoms  of  morbus  cordis  are  sometimes  referred  mainly  to 
the  heart  itself,  but  more  often  they  are  ascribed,  for  the  most  partj 

16 


METHODS   OF   DIAGNOSIS 


17 


to   other  organs,  consequent  on  the  disturbance  of  function  that 
attends  any  mechanical  derangement  of  their  blood  supply. 

A  systemic  arrangement  of  the  symptoms  will  be  adopted  in  the 
following  brief  account  of  the  subject. 

Cardio-vascular  system. ^ — Apart  from  pericarditis  and  angina 
pectoris,  prsecordial  pain  is  seldom  a  prominent  feature  of  heart 
disease.  A  feeling  of  tightness,  uneasiness,  or  pressure  in  the 
cardiac   region,   accompanied    possibly   by   palpitation,  or    by   the 


Palpation 


Percussion 


lnspecl"ron 


Symptomatology 


Auscultation 


Aetiology 


Diagnosis 


FIG.    7.      DIAGRAMMATIC   REPRESENTATION   OF  THE   DIAGNOSIS 

consciousness  of  an  irregular  or  intermittent  action  of  the  heart, 
is  sometimes  complained  of. 

These  symptoms  are,  however,  more  commonly  due  to  nervous 
causes,  or  to  digestive  disorders,  than  to  organic  disease  of  the  heart. 

Pulsation  may  be  felt  in  various  situations,  more  particularly 
in  the  region  of  the  head  and  neck,  and  is  occasionally  a  source 
of  much  discomfort. 

Noises  in  the  ears  are  also  experienced  in  connection  with 
abnormal  conditions  of  the  circulation. 

Hemorrhage  from  the  nose,  lungs,  stomach,  uterus,  etc.,  is  by 
no  means  uncommon,  and  may  lead  to  serious  loss  of  blood. 

Defective  supply  of  blood  to  the  extremities  is  the  cause  of  the 


i8  DISEASES   OF  THE   HEART 

cold  hands  and  feet  so  commonly  complained  of  by  the  subjects 
of  heart  disease.  Cyanosis  and  dropsy  will  be  considered  under  the 
heading  of  physical  methods  of  diagnosis  {vide  Inspection). 

Accidental  symptoms,  due  to  the  emboHc  plugging  of  an  artery  in 
the  brain,  spleen,  kidneys,  or  elsewhere,  may  occur  at  any  period  of 
the  disease. 

Bespiratory  system. — Shortness  of  breath  on  exertion  is  one 
of  the  earliest  indications  of  commencing  failure  of  the  muscular 
power  of  the  heart.  The  dyspnoea,  which  is  at  first  excited  and 
increased  by  effort,  gradually  becomes  more  pronounced  as  the 
cardiac  weakness  progresses,  and  in  the  final  stages  of  the  disorder 
may  culminate  in  orthopncea. 

In  some  instances  the  patient  suffers  from  paroxysmal  attacks  of 
difficulty  in  breathing,  which  are  known  under  the  name  of  cardiac 
asthma. 

Rhythmic  dyspnoea,  in  the  form  of  Cheyne-Stokes'  respiration, 
may  precede  the  fatal  event. 

The  pathology  of  cardiac  dyspnoea  will  be  discussed  subsequently. 

Cough,  with  a  variable  quantity  and  quality  of  expeetoration,  is 
often  a  troublesome  symptom. 

Haemoptysis  may  occur  more  especially  in  mitral  disease,  and 
epistaxis  is  not  uncommon  in  association  with  aortic  insufficiency. 

The  subjects  of  heart  disease  are  particularly  Hable  to  attacks  of 
bronchitis,  and  in  a  less  degree  to  pneumonia. 

Digestive  system. — It  frequently  happens  that  patients  suffering 
from  morbus  cordis,  notably  in  the  form  of  mitral  disease,  seek 
medical  advice  in  the  first  instance  for  the  relief  of  dyspepsia. 

The  derangement  of  digestion  usually  takes  the  form  of  epigastric 
pain,  or  weight  after  food,  nausea,  vomiting,  pyrosis,  flatulence,  and 
constipation,  or  irregular  action  of  the  bowels.  Flatulent  distension 
of  the  stomach  reacts  unfavourably  on  the  heart  by  directly  interfer- 
ing with  its  free  action,  and  in  this  way  gives  rise  to  palpitation  and 
cardiac  distress. 

Congestion  of  the  portal  circulation  is  commonly  associated  with 
a  greater  or  less  degree  of  gastro-intestinal  catarrh,  which  seriously 
aggravates  the  pre-existing  dyspepsia. 

Hsematemesis  sometimes  occurs,  and  hemorrhoids  are  frequently 
a  cause  of  very  great  discomfort. 

Pressure  on  the  oesophagus,  with  difficulty  in  swallowing,  may  be 
due  to  a  large  pericardial  effusion.  Hoarseness  or  aphonia  occasion- 
ally depends  on  a  like  cause. 

Nervous  system. — A  feeling  of  depression  and  languor,  dis- 
inclination for  mental  or  bodily  exertion,  pain  in  the  back  and 
extremities,  and  weakness,  twitching,  and  tremor  of  the  muscles  are 
among  the  early  indications  of  a  defective  supply  of  blood  to  the 
central  nervous  system. 


METHODS   OF   DIAGNOSIS  19 

Headache,  giddiness,  noises  in  the  ears,  flashes  of  hght  before 
the  eyes,  and  attacks  of  faintness  or  syncope  are  associated  with 
disturbance  of  the  cerebral  circulation. 

Sleeplessness  is  frequently  a  most  distressing  feature  of  diseases  of 
the  heart.  On  the  other  hand,  drowsiness  may  be  complained  of, 
and  sleep  is  often  attended  by  unpleasant  dreams.  DeUrium  is 
occasionally  observed,  and  is  of  serious  import. 

Emotional  disturbances,  mental  changes,  failure  of  memory, 
hallucinations,  melancholia,  dementia,  etc.,  are  not  infrequently 
found   in  association  with   the  different   forms  of   valvular  disease. 

Hemiplegia,  coma,  and  convulsions  may  be  due  to  haemorrhage  in 
the  brain  from  rupture  of  a  blood  vessel,  to  embolism  of  a  cerebral 
artery,  or  to  thrombosis  in  the  cerebral  veins. 

The  mode  of  onset  of  the  symptoms  considered  in  relation  to 
the  circulatory  conditions  at  the  time  of  their  occurrence,  the  age  of 
the  patient,  and  the  associated  causal  indications  outside  the  nervous 
system,  are  the  chief  points  in  the  differential  diagnosis  of  these 
lesions. 

Genito-urinary  system.  —  The  urine  of  heart  disease  (after 
failure  of  the  organ)  is  scanty,  high  coloured,  and  throws  down  on 
cooling  a  copious  deposit  of  urates. 

It  frequently  contains  albumen,  hyaline  or  granular  casts,  bile, 
uric  acid  crystals,  and  occasionally  blood.  The  characters  of  the 
urine  of  heart  disease  will  be  more  fully  considered  under  the 
heading  of  physical  diagnosis  {vide  Inspection). 

SECTION    II 

-STIOLOGY 

The  influence  of  the  age,  sex,  occupation,  and  history  of  the 
patient  on  the  incidence  of  heart  disease  will  be  considered  under 
their  respective  headings. 

Age. — Developmental  malformations,  and  intra-uterine  endo- 
carditis account  for  the  large  majority  of  cardiac  affections  that 
are  found  during  infancy. 

In  childhood,  endocarditis,  and  pericarditis,  of  rheumatic  origin, 
are  comparatively  common,  and  are  apt  to  run  a  very  insidious 
course.  The  rheumatic  symptoms  are  usually  slight,  and  unless 
great  watchfulness  is  exercised  may  easily  escape  observation.  The 
influence  of  chorea,  a  common  disorder  of  childhood,  in  the 
production  of  endocarditis,  is  largely  due  to  its  rheumatic  ancestry. 

Certain  of  the  acute  specific  fevers,  notably  scarlet  fever, 
diphtheria,  influenza,  pyaemia,  sepiicsemia,  and  measles  are  some- 
times accompanied  by  inflammatory  affections  of  the  heart. 

The  endocardial  inflammation  in  childhood  usually  attacks  the 
mitral  valve,  rarely  the  aortic.  During  adolescence  and  early  adult 
life  (15-30)  the  acute  inflammatory  affections  of  the  heart,  due  to 


20  DISEASES    OF   THE    HEART 

rheumatism,  are  more  prevalent  than  at  any  other  time.  Further- 
more, at  this  period  the  influence  of  anaemia  in  the  production  of 
cardiac  disease  is  most  marked,  and  at  the  same  time  functional 
disorders  of  the  heart  begin  to  make  their  appearance. 

The  mitral  valve  is  more  commonly  affected  than  the  aortic,  but 
the  relative  immunity  of  the  latter  is  not  so  great  during  this  stage 
as  in  childhood. 

Although  the  influences  just  mentioned  are  still  operative,  the 
middle  period  of  adult  life  (30-45)  introduces  other  important 
causes  of  cardiac  disease,  chief  among  which  are  physical  overstrain, 
syphilis,  and  many  other  toxcemias,  including  the  effects  of  excess  in 
the  use  of  alcohol  and  tobacco.  Moreover,  the  effects  on  the  heart 
and  aorta  of  the  high  arterial  tension  that  is  associated  with  gout, 
contracted  granular  kidney,  chronic  lead  poisoning,  emphysema, 
etc.,  commonly  begin  to  make  their  appearance  during  this  and  the 
succeeding  decade  of  life. 

In  later  adult  life  and  during  old  age  (45  and  upwards)  degenera- 
tive diseases  of  the  heart  and  aorta  become  increasingly  prevalent. 
True  angina  pectoris  rarely  occurs  before  the  age  of  40,  and  may 
therefore  be  fairly  included  among  the  cardiac  lesions  of  the  period 
under  consideration. 

Atheromatous  affections  of  the  endocardium  may  be  primary,  or 
they  may  be  grafted  on  to  pre-existing  valvular  disease. 

The  myocardium  is  frequently  the  seat  of  parenchymatous,  fatty, 
or  fibroid  changes,  as  well  as  of  other  nutritional  disturbances  of  a 
less  defined  nature,  which  are  closely  concerned  in  the  production 
of  failure  of  the  heart,  and  dilatation  of  its  cavities. 

Sex. — Women  suffer  more  frequently  from  chorea,  anaemia,  ex- 
ophthalmic goitre,  and  functional  affections  of  the  nervous  system 
than  men,  and  are  consequently  more  liable  to  the  cardiac  lesions 
associated  with  these  morbid  conditions.  On  the  other  hand,  the  in- 
fluence of  muscular  overstrain,  gout,  syphilis,  and  alcoholism  on  the 
incidence  of  heart  disease  is  more  marked  among  males  than  females. 

Occupation. — Persons  who  are  exposed  to  cold  and  wet,  as  for 
instance  washerwomen,  out-door  labourers,  cabmen,  etc.,  are  more 
liable  to  suff"er  from  the  rheumatic  manifestations  of  heart  disease 
than  other  people. 

All  occupations  that  are  attended  by  severe  muscular  exertion, 
and  more  especially  those  that  entail  sudden  effort,  are  productive 
of  enlargement  of  the  heart,  and,  if  the  cause  persist,  of  aortic  and 
arterial  disease,  in  the  form  of  arterio-sclerosis  and  atheroma. 

These  conditions  obtain  principally  among  hammermen,  miners, 
stokers,  hill-climbers,  puddlers,  stonemasons,  slaughterers,  soldiers, 
and  sailors,  and  to  a  less  degree  among  athletes. 

In  the  case  of  soldiers,  and  possibly  in  other  instances,  it  is 
probable  that  a  nervous  element  co-operates  with  the  muscular 
overstrain  in  the  production  of  the  cardiac  hypertrophy. 

The  enlargement  of  the  heart,  in  the  class  of  cases  under  con- 


METHODS    OF   DIAGNOSIS  2\ 

sideration,  is  due  predominantly  either  to  hypertrophy  or  to  dilatation 
according  as  the  state  of  cardiac  nutrition  is  satisfactory  or  otherwise. 
Hypertrophy  of  the  left  ventricle  is  the  condition  usually  found. 

Aortic  valvular  disease,  arterio-sclerosis,  and  atheroma  are  due  to 
the  strain  to  which  the  whole  arterial  system  is  exposed  in  cases  of 
prolonged  muscular  exertion. 

Persons  of  sedentary  habits,  who  habitually  eat  and  drink  to 
excess,  are  frequently  the  subjects  of  atheromatous  disease  and  of 
myocardial  degeneration. 

History. — -A  short  account  will  be  given  under  this  heading  of 
the  various  conditions  of  disease,  and  other  morbid  influences  in 
the  life-history  of  the  patient  that  are  causally  related  to  affections 
of  the  heart. 

Rheumatism,  in  one  or  other  of  its  manifold  phases,  is  by  far  the 
most  important  cause  of  heart  disease.  In  many  instances  it  is 
possible,  indeed  probable,  that  the  cardiac  affection  is  the  sole 
manifestation  of  the  rheumatic  state.  The  endocardium,  pericardium, 
and  myocardium  may  be  separately  or  simultaneously  the  seat  of 
acute  or  chronic  inflammatory  changes  in  rheumatic  cases.  Endo- 
carditis and  pericarditis  also  arise  in  connection  with  certain  of  the 
specific  fevers,  notably  with  scarlet  fever,  less  frequently  with 
measles  and  erysipelas,  and  rarely  with  enteric  fever  and  small- 
pox. Inflammation  of  the  pericardium  is  a  comparatively  common 
complication  of  chronic  Bright's  disease,  and  it  is  occasionally 
observed  in  the  course  of  pysemia  and  pneumonia. 

Malignant  endocarditis,  which  in  three-fourths  of  the  cases  is 
superimposed  on  previously  existing  valvular  disease,  occurs  in  asso- 
ciation with  pneumonia,  puerperal  fever,  osteomyelitis,  the  specific 
fevers,  phlebitis,  and  with  other  forms  of  septicemia  and  pyjemia. 

Pysemia  and  phlebitis  also  account  for  a  certain  number  of  the 
cases  of  acute  myocarditis. 

The  so-called  "parenchymatous  myocarditis"  appears  in  the 
course  of  many  of  the  acute  febrile  and  infective  processes,  as  for 
instance  enteric  fever,  diphtheria,  scarlatina,  small-pox,  typhus, 
relapsing  fevers,  septicaemia,  and  pyaemia. 

Anaemia  is  a  frequent  cause  of  cardiac  malnutrition  and  dilata- 
tion of  the  heart,  which  usually  disappear  with  the  restoration  of 
a  normal  blood  condition. 

The  comparatively  common  occurrence  of  mitral  stenosis  among 
women  in  the  absence  of  a  history  of  rheumatism  has  led  to  the 
belief  that  chlorosis  may,  in  some  instances,  be  a  cause  of  this 
form  of  organic  valvular  disease. 

Gout,  chronic  alcohoUsm,  and  syphilis  are  among  the  chief  dis- 
posing causes  of  aortic  valvular  lesions,  arteritis,  and  atheromatous 
affections  of  the  arterial  system.  Degenerative  changes  in  the 
myocardium,  of  a  fatty  and  fibroid  nature,  are  also  frequently 
associated  with  alcoholism,  syphilis,  and  other  toxaemias. 


22  DISEASES   OF   THE   HEART 

Physical  overstrain  and  protracted  high  arterial  tension  from  any 
cause  are  productive  of  enlargement  of  the  heart,  and  of  arterial 
disease  in  the  form  of  aortic  valvular  lesions,  arterio-sclerosis,  and 
atheromatous  affections.  Nervous  disorders  of  the  heart  frequently 
owe  their  origin,  in  part  at  least,  to  physical  overstrain. 

Worry,  anxiety,  grief,  and  long-continued  mental  strain  of  any  kind 
are  sometimes  the  exciting  cause  of  cardiac  disease,  and  their  occur- 
rence adds  greatly  to  the  gravity  of  pre-existing  affections  of  the  heart. 

The  influence  of  heredity  on  the  incidence  of  heart  disease  has 
also  to  be  taken  into  consideration.  Cardiac  affections  are 
hereditary  chiefly  in  so  far  as  their  causes  are  hereditary.  Thus 
rheumatism  and  gout,  on  which  the  large  majority  of  the  cases  of 
heart  disease  depend,  show  a  remarkable  tendency  to  be  trans- 
mitted from  one  generation  to  another.  An  hereditary  tendency 
to  high  arterial  tension  and  atheroma  is  also  observed  in  some 
cases.  The  functional  derangements  of  the  heart  which  depend  on 
neuroses  of  various  kinds  are  likewise  prone  to  run  in  families. 

SECTION    III 

THE   PHYSICAL   METHODS   OF   DIAGNOSIS 

So  far  as  the  examination  of  the  heart  is  concerned,  the  physical 
methods  of  diagnosis  range  themselves  under  the  four  heads  of 
Inspection,  Palpation,  Percussion,  and  Auscultation,  which,  as 
previously  mentioned,  should  always  be  practised  in  this  order. 
The  data  afforded  by  each  of  these  methods  will  first  be  given  in 
tabular  form,  and  then  discussed  in  detail. 

SUB-SECTION  I 

INSPECTION 

No  complete  or  accurate  physical  examination  of  the  heart  is 
possible  unless  the  entire  chest  is  fully  exposed. 

The  information  afforded  by  inspection  may  be  most  conveniently 
classified  under  the  two  heads  of 

A.  General    B.  Local 

A.  General. — This  will  be  considered  under  the  followin 
scheme  :  (^^-^  Appearance  a?id  attitude  of  the  patient 

(b)   Colour 

1.  Cyanosis  or  lividity 

2.  Pallor 

3.  Jaundice 
{c)   Dyspncea 

(d)  Dropsy 

(e)  State  of  gefieral  nutrition 
(/)  Urifie 


METHODS   OF  DIAGNOSIS  23 

B.  Local. — This  will  be  discussed  under  the  following  arrange- 
ment : — 

{a)  Bulging  or  retraction  of  the  prcecordial  region  as  a  whole,  or 

in  part 
(b)  Position  of  the  apex  beat 
{c)    Visible  pulsation 

1.  Cardiac 

Prsecordium  as  a  whole,  or  in  part 

Epigastric 

Displaced 

2,  Vascular 

Arterial 
Venous 
Capillary 
Glandular 

A.    GENERAL 

{a)  Appearance  and  Attitude 

The  aspect  of  the  patient  suffering  from  morbus  cordis  is  often 
very  characteristic,  and  it  should  be  noted  in  all  cases.  The  facial 
appearance  commonly  associated  with  the  more  important  cardiac 
lesions  will  be  fully  described  under  their  respective  headings.  The 
attitude  of  the  patient  is  frequently  peculiar  to  his  condition,  and 
may  have  considerable  diagnostic  significance. 

{b)  Colour 

I.  Cyanosis  or  lividity. — This  phenomenon,  with  clubbing  of  the 
fingers  and  toes,  and  coldness  of  the  extremities,  is  usually  associated 
with  congenital  malformations  of  the  heart.  It  is,  however,  also 
observed,  though  usually  to  a  less  marked  extent,  in  chronic  disease 
affecting  the  mitral  and  tricuspid  valves,  and  in  lesions  of  the  cardiac 
walls.  Cyanosis,  to  any  great  degree,  is  rarely  found  independently 
of  some  form  of  heart  disease.  The  discolouration  of  the  skin  in  any 
given  case  is  seldom  constant,  and  may  vary  within  very  wide  limits. 
It  is  increased  by  excitement,  exertion,  and  lung  complications, 
and  diminishes  under  the  influence  of  rest,  sleep,  etc. 

Two  theories  have  been  advanced  with  the  object  of  explaining 
the  mode  of  production  of  the  cyanosis.  The  one,  proposed  by 
Morgagni,  attributes  the  blue  tint  to  the  general  venous  congestion 
caused  by  the  obstruction  to  the  free  passage  of  blood  through  the 
right  side  of  the  heart;  while  the  other,  advanced  by  Hunter, 
ascribes  it  to  the  intermixture  of  venous  and  arterial  blood.  Both 
views  have  met  with  wide  acceptance.  There  are,  however,  several 
very  powerful  arguments  which  favour  the  explanation  afforded  by 
Morgagni's  theory.  It  has,  in  the  first  place,  been  clearly  shown 
that  no  constant  relation  exists  between  the  intensity  of  the  cyanosis 
and  the  amount  of  intermixture  of  arterial  and  venous  blood ;  more- 


24  DISEASES  OF  THE  HEART 

over,  extreme  cyanosis  may  exist  without  any  possibility  of  inter- 
mixture. Furthermore  it  is  noteworthy  that  in  all  cases  of  well 
marked  cyanosis  the  conditions  under  which  great  venous  obstruction 
may  occur  are  present. 

It  would  appear,  therefore,  that  Morgagni's  theory  affords  a  fairly 
adequate  explanation  of  the  manner  in  which  cyanosis  is  produced. 
At  the  same  time  it  is  probable  that  the  intensity  of  the  cutaneous 
discoloration  is  influenced  by  other  factors,  such  as  the  amount  of 
intermixture  of  arterial  and  venous  blood ;  an  insufficient  aeration  of 
blood  by  the  lungs ;  dilatation  of  the  cutaneous  capillaries  and  an 
unusual  transparency  of  the  skin. 

2.  Pallor. — The  frequent  association  of  anaemia  with  morbus 
cordis  is  a  matter  of  common  observation,  and  its  production, 
excluding  accidental  causes  such  as  epistaxis,  hsemoptysis,  menor- 
rhagia,  etc.,  is  accounted  for  in  two  ways,  viz  : — 

1.  That   the   chief  causes   of   heart   disease,    as,    for    instance, 

rheumatism,  the  specific  fevers,  gout,  etc.,  site  per  se  fruitful 
sources  of  ansemia. 

2.  That   in   consequence  of  the   particular  lesion   which  exists, 

the  circulation  is  inadequately  maintained,  and  the  proper 
assimilation  of  food  and  elimination  of  waste  products  is 
more  or  less  defective,  and  hence  the  anemia. 

The  most  intense  form  of  anaemia  resulting  from  organic  disease 
of  the  heart  is  that  associated  with  aortic  incompetence.  Children 
suffering  from  morbus  cordis  are  frequently  the  subjects  of  severe 
anaemia  induced  by  repeated  attacks  of  rheumatism. 

The  pallor  affects  the  general  surface  of  the  skin,  the  conjunctivae, 
and  mucous  membranes. 

3.  Jaundice. — This  sign,  which  is  seldom  well-marked  or  constant, 
is  usually  observed  after  failure  of  the  heart,  and  most  commonly 
with  mitral  and  tricuspid  lesions.  During  the  early  stages  of  cardiac 
failure  the  jaundice  is  due  to  catarrh  of  the  bile  ducts,  while  at  a 
later  period  of  the  disease  it  depends  on  organic  changes  in  the 
liver,  the  result  of  long-continued  venous  congestion. 

{c)  Dyspnoea 

Dyspnoea,  by  which  is  meant  increased  action  of  the  respiratory 
muscles,  both  as  regards  frequency  and  degree  of  contraction,  may 
be  either  inspiratory  or  expiratory,  or  a  combination  of  the  two 
conditions. 

Speaking  generally,  cardiac  dyspnoea  is  both  inspiratory  and 
.  expiratory. 

With  disease  of  the  heart  difficulty  of  breathing  may  be  observed 
under  several  conditions  : — 

I.  It  may  appear  on  exertion  only,  or  as  the  result  of  some  other 
external  influence. 


METHODS   OF   DIAGNOSIS  25 


2. 


It  may  arise  spontaneously,  or  without  any   obvious   exciting 
cause. 

3.  It   may  be  constant  and   postural,  and   it  is  then   known  as 

orthopncea. 

4.  It  may  be  paroxysmal,  or  rhythmic,  in  the  form  of — 

(a)  Cardiac  asthma 

(d)  Cheyne-Stokes'  respiration. 

The  value  of  dyspnoea  as  an  indication  of  failure  of  the  heart 
depends  on  the  magnitude  of  the  cause  producing  it.  Dyspnoea 
which  arises  spontaneously,  or  as  the  result  of  very  slight  provoca- 
tion, argues  a  greater  degree  of  cardiac  insufficiency  than  that  pro- 
duced by  some  definite  and  partially  adequate  cause.  Orthopncea, 
often  associated  with  dropsy,  usually  indicates  a  considerable 
amount  of  dilatation  of  the  heart  from  failure.  The  occurrence 
of  Cheyne-Stokes'  respiration  with  organic  disease  of  the  heart  is 
usually  but  not  invariably  of  fatal  import. 

The  pathology  of  dyspnoea,  though  somewhat  complicated,  can 
be  but  briefly  considered. 

The  movements  of  respiration  are  regulated  by  the  respiratory 
centre,  the  activity  of  which  depends  on  the  quantity  and  quality 
of  blood  supplied  to  it.  An  excess  of  carbon  dioxide,  or  a 
deficiency  of  oxygen  in  the  blood,  excites  the  centre  to  greater 
activity,  with  the  result  that  increased  action  of  the  respiratory 
muscles  is  produced,  or,  in  other  words,  dyspnoea. 

Now,  in  disease  at  the  mitral  orifice  there  is  always,  owing  to 
the  position  of  the  opening,  more  or  less  embarrassment  of  the 
pulmonary  circulation,  whereby  the  blood  becomes  insufficiently 
aerated,  z'.e.  it  contains  more  carbon  dioxide  and  less  oxygen 
than  normal,  and  the  consequent  stimulation  of  the  respiratory 
centre  gives  rise  to  dyspnoea. 

This  explanation,  however,  of  the  cause  of  cardiac  dyspnoea  is 
probably  far  from  covering  the  whole  of  the  ground. 

A  venous  condition  of  the  blood  produces,  also,  through  its 
effect  on  the  vaso-motor  centre,  a  general  rise  of  systemic  blood 
pressure  by  virtue  of  the  contraction  of  the  arterioles  throughout 
the  body.  Von  Basch  has  shown  that  increased  systemic  tension 
is  invariably  followed  by  a  rise  of  blood  pressure  in  the  pulmonary 
circulation.  He  also  points  out  that  the  accompanying  distension 
of  the  pulmonary  capillaries  causes,  so  to  speak,  a  general  erection 
of  the  lung  tissue,  with  enlargement  of  the  lumina  of  the  alveoli, 
and  increased  rigidity  of  their  walls.  As  a  consequence  of  these 
changes,  increased  inspiratory  force  is  required  to  properly  inflate 
the  lungs,  and  expiration  is  difficult  owing  to  the  impairment  of 
the  elasticity  of  the  alveolar  walls,  hence  dyspnoea  follows  in 
proportion  to  the  difficulties  to  be  overcome. 

It  would  therefore  appear  probable  that  in  the  production  of 
cardiac    dyspnoea,    pulmonary    engorgement    acts    in    two    ways : 


26  DISEASES   OF   THE    HEART 

(a)  directly  by  a  mechanical  effect  on  the  lungs,  and  (i)  indirectly 
through  the  respiratory  centre. 

Dyspnoea  produced  by  cardiac  insufficiency  assists  the  circu- 
lation inasmuch  as  each  respiration  pumps  the  blood  from  the 
venous  system  through  the  lungs  (Leonard  Hill). 

The  foregoing  account,  while  offering  a  fairly  adequate  explana- 
tion of  the  causes  of  dyspnoea  in  disease  at  the  mitral  orifice,  does 
not  by  any  means  exhaust  the  subject. 

In  pulmonic  and  tricuspid  valvular  lesions  the  mechanical  inter- 
ference with  the  circulation  through  the  right  heart  and  lungs  will 
result  in  the  insufficient  aeration  of  the  blood  and  the  consequent 
stimulation  of  the  respiratory  centre  with  the  production  of  dyspnoea. 

In  disease  at  the  aortic  orifice  shortness  of  breath  is  always  a 
prominent  feature.  Its  production  probably  depends  on  several 
factors,  chief  among  which  are  (i)  the  anaemia  that  is  commonly 
associated  with  these  lesions,  and  (2)  the  interference  with  the  proper 
supply  of  blood  to  the  heart  and  medulla,  owing  to  the  degenerative 
changes  (arterio- sclerosis  and  atheroma)  in  the  walls  of  the  arteries 
supplying  these  structures,  which  are  affected  in  common  with  the 
other  arteries  of  the  body  in  cases  of  aortic  valvular  disease. 

In  the  production  of  cardiac  dyspnoea  an  additional  factor  still 
remains  to  be  mentioned,  and  that  is  the  reflex  disturbance  of  the 
nervous  mechanism  of  respiration  which  must  occur,  to  a  greater 
or  less  degree,  in  all  cases.  Its  influence  is  more  obvious  in  the 
dyspnoea  associated  with  disease  of  the  aorta  and  its  orifice  and 
of  the  cardiac  walls  than  of  any  other  heart  structure. 

The  precise  manner  in  which  this  reflex  effect  is  produced  and 
the  circumstances  under  which  its  action  is  brought  into  play  have 
not  yet  received  an  adequate  explanation,  but  there  can  be  no 
doubt  that  sensory  nerves  supplying  the  heart,  great  vessels,  and 
lungs  are  involved  in  the  morbid  processes  affecting  these  structures. 

A  striking  example  of  the  reflex  production  of  severe  dyspnoea 
independently  of  pulmonary  influences  is  seen  in  cases  of  acute 
inflammation  of  the  aorta. 

Orthopnoea  is  the  condition  in  which  the  patient  is  obliged 
to  adopt  a  semi-erect  or  sitting  position,  since  any  attempt  to  lie 
down  is  followed  by  severe  and  insupportable  dyspnoea.  The 
attitude  of  the  patient  is  often  peculiar  to  this  form  of  laboured 
breathing,  and  is  such  that  he  can  bring  into  action  the  accessory 
muscles  of  respiration  to  the  greatest  possible  advantage.  The 
upright  position  also  facilitates  the  movements  of  the  diaphragm, 
by  reason  of  the  descent  of  the  liver,  and  other  abdominal  organs 
under  the  influence  of  gravity,  and  the  same  force  may  also  retard 
the  flow  of  blood  in  the  inferior  vena  cava,  and  by  this  means 
relieve  the  engorgement  of  the  right  heart  and  pulmonary  circulation. 

The  significance  of  orthopnoea  has  already  been  indicated. 

The  cause  of  cardiac  asthma  has  not  yet  been  fully  determined, 
though  doubtless  in  many  instances  it  is  due  to  toxic  influences, 
the  result  of  defective  eUmination  by  the  kidneys. 


METHODS   OF   DIAGNOSIS  27 

The  pathology  of  Cheyne-Stokes'  respiration  is  still  uncertain, 
though  speaking  generally  the  phenomenon  is  attributable  to 
exhaustion  of  the  respiratory  centre,  and  the  consequent  deterioration 
of  functional  activity  finds  expression  in  a  less  speciahzed  form  of 
energetical  manifestation,  which,  as  in  the  case  of  all  vital  phenomena 
under  similar  conditions,  tends  to  assume  a  rhythmical  or  periodic 
type. 

{d)  Dropsy- 
Dropsy  of  cardiac  origin  almost  invariably  begins  in  those  portions 
of  the  body  which  are  most  distant  from  the  heart.  It  commences, 
therefore,  in  the  feet  and  legs  and  gradually  spreads  upwards.  At  an 
early  period  it  invades  parts  like  the  scrotum  and  eyelids,  where  the 
subcutaneous  tissues  are  looser,  and  the  vessels  less  supported  than 
elsewhere.  Ultimately  all  the  subcutaneous  tissues  may  become 
infiltrated  with  fluid. 

Effusion  into  the  peritoneal  and  pleural  cavities  is  not  uncommon, 
and  may  occur  at  a  comparatively  early  stage  of  the  cardiac  failure. 
The  pericardium  is  affected  less  frequently,  and  usually  at  a  later 
period  of  the  disease. 

Dropsy  may  be  observed  in  almost  any  form  of  heart  disease,  but 
it  is  most  commonly  associated  with  mitral  and  tricuspid  lesions, 
and  with  affections  of  the  cardiac  walls. 

The  pathology  of  cardiac  dropsy  is  briefly  as  follows  : — 
In  consequence  of  {a)  the  enfeeblement  of  the  driving  power  of 
the  ventricles  and  {b)  the  obstruction  to  the  onward  flow  of  blood 
through  the  right  side  of  the  heart,  a  condition  of  systemic  venous 
engorgement  is  produced  which  leads  to  a  general  rise  of  intra- 
venous and  capillary  pressure.  This  state  of  the  circulation  favours 
an  increased  transudation  of  the  fluid  elements  of  the  blood  from  the 
smaller  vessels  and  capiUaries  into  the  connective  tissue  and  lymph 
spaces,  and  a  diminished  re-absorption  from  them  into  the  venous 
radicles.  The  process  is  in  all  probability  intensified  by  changes  in 
the  composition  of  the  blood,  and  by  the  consequent  interference 
with  the  nutrition  of  the  Hning  membrane  of  the  capillaries  and 
smaller  vessels. 

Under  physiological  conditions  the  lymph  channels  alone  would 
suffice  to  carry  off  the  increased  quantity  of  fluid  exuded  from  the 
capillaries,  but  the  lymph  circulation  is  also  impeded,  owing  to 
{a)  the  general  muscular  enfeeblement,  {b)  the  diminished  aspirating 
power  of  the  thorax,  {c)  the  diminished  suction  power  of  the 
ventricles,  and  (d)  the  positive  intra-venous  pressure  in  the  great 
trunks  of  the  neck  and  thorax. 

As  the  result,  therefore,  of  the  general  venous  engorgement,  and 
the  impeded  lymphatic  circulation,  the  fluid  exuded  by  the  capillajies 
and  small  vessels  is  unable  to  escape  completely  by  either  venous  or 
lymphatic  outlet,  consequently  it  accumulates  in  the  subcutaneous 
tissues  and  spaces,  with  the  production  of  dropsy. 


28  DISEASES    OF   THE    HEART 

(<?)  State  of  General  Nutrition 

Lesions  of  the  mitral  valve  are  frequently  attended  by  considerable 
emaciation,  which  depends,  in  a  large  measure,  on  the  digestive 
derangements  and  the  malassimilation  of  food  associated  with  con- 
gestion of  the  portal  circulation. 

Aortic  disease  does  not,  as  a  rule,  give  rise  to  much  disturbance  of 
nutrition,  though  it  is  commonly  found  in  persons  of  spare  habit. 
Wasting,  accompanied  by  anaemia,  is  sometimes  a  prominent  feature 
of  heart  disease  in  children,  and  when  extreme  may,  in  conjunction 
with  the  respiratory  difficulties,  excite  a  suspicion  of  tuberculosis. 

Lesions  of  the  cardiac  wall  are  in  some  instances  found  in 
association  with  general  obesity. 

(/)  Urine 

The  urine  in  cases  of  morbus  cordis  presents  no  abnormal 
features  until  the  heart  fails.  With  the  onset  of  cardiac  failure 
it  becomes  scanty,  high-coloured,  and  shows  on  cooling  a  copious 
precipitate  of  urates.  Albumin  is  usually  present  in  small  quantity, 
and  increases  as  the  cardiac  disability  progresses.  The  specific 
gravity  of  the  urine  is  raised,  and  the  daily  excretion  of  urea  dimin- 
ished. The  occasional  presence  of  blood  in  the  urine  is  accounted 
for  by  the  rupture  of  congested  renal  capillaries. 

It  is  of  great  importance  to  distinguish  the  urine  associated  with 
failure  of  the  heart  from  that  due  to  acute  or  chronic  inflammatory 
affections  of  the  kidneys. 

The  latter  are  characterised  by  the  presence  of  casts  and  other 
renal  debris  in  the  urine. 

In  acute  inflammatory  conditions  of  the  kidney  the  urine  is 
scanty,  and  contains  a  variable  quantity  of  blood  and  large  amounts 
of  albumin  and  casts. 

In  chronic  Bright's  disease  the  urine  is  increased  in  amount,  and 
contains  little  albumin  and  a  variable,  though  usually  small,  number 
of  casts. 

The  general  manifestations  of  any  morbid  process  which  may 
injuriously  affect  the  heart  should  be  carefully  noted  during  this 
part  of  the  examination  of  the  patient. 


B.   LOCAL 

{a)   Bulging  or  Retraction  of  the  Praecordial  Region 
as  a  Whole  or  in  Part 

Bulging  of  the  praecordial  area,  which  is  not  limited  by  the 
outline  of  the  heart,  may  be  due  to  rickets,  spinal  curvature, 
localized  empyema,  left  pleural  effusion,  or  to  inflammatory  con- 
ditions of  the  superficial  tissues.     The  diagnosis  of  the  cause  of  thx^ 


METHODS    OF    DIAGNOSIS  29 

prominence  in  cases  of  this  kind  rests  on  the  associated  symptoms 
and  physical  signs,  and  as  a  rule  presents  no  difificulties.  Undue 
prominence  of  the  praecordial  region  corresponding  with  the  out- 
line of  the  heart  is  most  commonly  caused  by  large  pericardial 
effusions  or  by  enlargement  of  the  heart  following  valvular  disease 
in  early  life.  Bulging  of  the  intercostal  spaces  in  the  cardiac  area 
with  widening  of  the  interval  between  them  is  almost  always  the 
result  of  pericardial  inflammation  with  effusion. 

Forward  displacement  of  the  heart  by  means  of  a  growth  or  other 
tumour  situated  behind  the  organ,  and  aneurism  of  the  first  portion 
of  the  aortic  arch,  are  also  occasional  causes  of  prgecordial  bulging. 

Flattening  of  the  precordial  region  not  limited  to  the  cardiac 
outline  may  be  due  to  congenital  malformation,  to  long-continued 
pressure,  as  in  the  case  of  shoemakers  and  joiners,  or  to  retraction 
of  the  left  lung. 

Retraction  of  the  prcccordium  caused  by  pericardial  adhesions  is 
usually  most  marked  over  the  lower  end  of  the  sternum  and  adjacent 
portion  of  the  left  infra-mammary  region.  General  prsecordial 
retraction  is  sometimes  due  to  universal  pericardial  adhesion,  the 
result  of  pericarditis  in  childhood. 

Bulging  or  retraction  of  the  prsecordial  region,  corresponding 
with  different  parts  of  the  heart's  area,  is  comparatively  rare,  and 
the  cause  of  the  condition  may  be  deduced  from  the  foregoing 
considerations. 

{b)  Position  of  the  Apex  Beat 

The  position  of  the  apex  beat  has  already  been  defined  (see 
p.  i).  The  apex  beat  under  normal  conditions  extends  over  an 
area  included  in  a  circle  with  a  radius  of  about  half  an  inch.  It 
may  be  displaced  from  either  {a)  intrinsic  or  {b)  extrinsic  causes. 

The  further  consideration  of  displacements  of  the  apex  beat  will 
be  found  under  the  headings  of  "  Palpation  "  and  "  Displacements 
of  the  Heart"  (see  pp.  34  and  35). 

{c)  Visible  Pulsation 

I.  Cardiac.  Prcecordium  as  a  whole  or  in  part. — General 
prsecordial  pulsation  of  a  diffused  wavy  character  may  often  be 
observed  in  children  with  valvular  disease,  more  especially  when 
associated  with  pericardial  adhesions.  A  similar  phenomenon  is 
occasionally  seen  in  adults  in  cases  of  cardiac  enlargement,  and  in 
those  conditions  in  which  the  heart  is  brought  into  closer  contact 
with  the  chest  wall  by  means  of  the  pressure  of  a  growth  or  other 
tumour  from  behind,  or  as  the  result  of  the  retraction  of  the  lungs. 

General  systolic  retraction  of  the  prsecordium  can  be  due  only  to 
universal  pericardial  adhesion. 

The  most  common  cause  of  pulsation  over  a  portion  of  the 
prsecordial  area  is  enlargement  of   the  left  ventricle,  and  the  pulsa- 


30  DISEASES   OF  THE   HEART 

tion  is  then  continuous  and  synchronous  with  the  apex  beat.  Pulsa- 
tion may  occur,  however,  in  this  situation  without  any  enlargement 
of  the  left  ventricle,  as  in  nervous  excitation  of  the  heart,  Graves' 
disease,  etc. 

Enlargement  of  the  right  ventricle  may  give  rise  to  pulsation 
between  the  left  edge  of  the  sternum  and  the  apex  beat. 

Pulsation  in  the  third  left  intercostal  space  close  to  the  sternum 
may  be  due  to  enlargement  of  the  left  auricle,  but  it  is  probably 
more  commonly  the  result  of  dilatation  of  the  infundibulum  of  the 
right  ventricle. 

An  enlarged  right  auricle  may  give  rise  to  visible  pulsation  in  the 
third  and  fourth  interspaces  to  the  right  of  the  sternum. 

Visible  auricular  pulsation  may  be  either  presystolic  or  systolic  in 
time,  but  in  the  majority  of  instances  it  is  systolic,  owing  to  reflux 
from  the  ventricles. 

Pulsation  in  the  third,  fourth,  and  fifth  left  intercostal  spaces 
between  the  sternal  edge  and  vertical  nipple  line  is  sometimes 
associated  with  anaemia,  and  may  also  depend  on  the  uncovering 
of  the  heart  by  reason  of  the  retraction  of  the  left  lung.  Indeed, 
it  may  be  stated  generally  that  the  presence  or  absence  of  prse- 
cordial  pulsation  largely  depends  on  the  extent  to  which  the  heart 
is  covered  by  lung  tissue. 

Systolic  retraction  of  the  fourth  and  fifth  intercostal  spaces  in  the 
region  of  the  apex  beat  is  often  associated  with  hypertrophied  con- 
ditions of  the  left  ventricle,  and  must  not  be  regarded  as  a  sign  of 
pericardial  adhesion. 

Systolic  retraction  of  the  ribs,  costal  cartilages,  or  sternum  is 
indicative  of  pericardial  adhesion.  Of  much  greater  importance, 
however,  in  the  diagnosis  of  this  condition  is  diastolic  retraction 
of  the  intercostal  spaces,  which  can  hardly  be  produced  by  anything 
but  pericardial  adhesion.  Systolic  and  diastolic  retraction  of  spaces 
may  be  associated. 

In  the  diagnosis  of  pericardial  adhesion  the  signs  afforded  by 
inspection  and  palpation  should  be  considered  together,  inasmuch 
as,  at  first  sight,  the  data  obtained  by  the  two  methods  appear  to  be 
contradictory,  i.e.  the  visible  recession  of  the  chest  wall  is  accom- 
panied by  a  palpable  impulse. 

Epigastric pichation. — This  phenomenon  can  be  produced  by  the 
forcible  pulsation  of  a  normal  right  ventricle,  such  as  is  occasioned 
by  simply  holding  the  breath,  or  by  any  temporary  pulmonary 
obstruction. 

Visible  epigastric  pulsation  commonly  means  either  enlargement 
(hypertrophy  and  dilatation)  of  the  right  ventricle,  or  displacement 
downwards  of  the  heart,  or,  as  in  pulmonary  emphysema,  a  com- 
bination of  the  two  conditions. 

Other  accidental  causes  of  epigastric  pulsation  are:  (i)  neurotic 
pulsation  of  the  abdominal  aorta ;  (2)  aneurism  of  the  upper  part 
of  the  abdominal  aorta,  or  a  tumour  in  front  of  this  portion  of  the 


METHODS   OF   DIAGNOSIS  31 

vessel ;  (3)  pulsation  of  the  liver ;  (4)  systolic  recession  of  the 
epigastrium  due  to  pericardial  adhesion. 

The  differential  diagnosis  of  the  cause  of  epigastric  pulsation  is 
not  usually  a  matter  of  any  great  difficulty. 

Immobility  of  the  upper  portion  of  the  epigastric  triangle  is, 
according  to  Sir  William  Broadbent,  always  associated  with  exten- 
sive pericardial  adhesion. 

Displaced  pulsation. — The  cardiac  impulse  may  be  displaced  up- 
wards or  downwards,  to  the  right  or  left,  conformably  with  altera- 
tions in  the  position  of  the  heart.  In  extreme  instances  there  is  a 
complete  absence  of  pulsation  over  the  normal  situation  of  the 
organ,  which  may  be  seen  beating  in  some  unusual  position. 

The  causes  of  displacement  of  the  heart  will  be  considered  under 
the  heading  of  "  Palpation." 

2.  Vascular  pulsation.  Arlerial pulsalion.—I'ulsa.tion  above  the 
level  of  the  third  rib,  if  systolic  in  time,  is  generally  of  arterial 
origin. 

If  in  the  second  right  intercostal  space,  close  to  the  sternum,  it  is 
probably  due  to  dilatation  of  the  ascending  portion  of  the  aorta.  If 
in  the  second  left  interspace,  the  cause  is  usually  exposure  of  the 
pulmonary  artery  owing  to  retraction  of  the  left  lung. 

Pulsation  due  to  aneurism  of  the  arch  of  the  aorta  may  appear  to 
the  right  or  left  of  the  sternum,  or  in  the  episternal  notch  and  middle 
line,  according  to  the  part  of  the  vessel  that  is  affected.  Pulsation 
in  the  episternal  notch  may  be  visible  under  perfectly  normal  con- 
ditions. 

Aneurism  of  the  innominate  artery  may  give  rise  to  pulsation  in 
the  neighbourhood  of  the  sternal  end  of  the  right  clavicle. 

Pulsation  due  to  aneurism  of  the  subclavian  arteries  may  appear 
above  or  below  the  clavicle.  The  presence  of  pulsation  beneath 
the  outer  ends  of  either  clavicle,  often  visible  in  thin  subjects,  is  of 
no  clinical  importance. 

Visible  and  forcible  pulsation  of  the  arteries  at  the  root  of  the 
neck  may  occur  under  many  conditions.  It  is  commonly  seen  in 
nervous  affections  of  the  heart,  in  anaemia,  and  after  great  exertion 
or  mental  excitement. 

Visible  pulsation  of  the  arteries  generally  is  particularly  charac- 
teristic of  aortic  insufficiency,  and  is  then  often  associated  with  a 
locomotion  forwards  of  the  vessels.  The  latter  phenomenon  is  well 
seen  in  the  case  of  the  temporal  arteries  which,  in  addition  to  the 
forward  displacement,  undergo  a  peculiar  vermicular  movement  with 
each  beat  of  the  heart. 

A  similar  condition,  though  very  much  less  marked,  may  occa- 
sionally be  seen  in  the  arteries  of  old  people  in  whom  the  arterial 
wall  is  rigid,  and  the  contraction  of  the  left  ventricle  sudden  and 
badly  sustained. 


32  DISEASES    OF   THE    HEART 

Venous  pulsation. — Except  in  some  cases  of  anaemia  and  chlorosis, 
and  in  rare  instances  in  healthy  people,  pulsation  in  the  veins  of  the 
neck  is  accompanied  by  venous  distension.  Apart  from  these  excep- 
tions venous  pulsation  is  either  auriculo-systolic  or  ventriculo-systolic, 
or  both,  and  is  indicative  of  obstruction  at  the  tricuspid  orifice,  or 
of  incompetence  of  its  valve.  The  most  common  cause  of  venous 
pulsation  in  the  neck  is  incompetence  of  the  tricuspid  valve,  the 
result  of  failure  of  the  right  ventricle.  Tricuspid  incompetence 
may  exist  without  venous  pulsation,  provided  the  amount  of  regurgi- 
tation is  slight,  and  the  venous  valves  remain  competent ;  and,  con- 
versely, slight  pulsation  may  occur  in  the  veins  of  the  neck  without 
any  tricuspid  incompetence,  the  pulsation  being  the  result  of  the 
auricular  systole,  or  of  the  vibration  of  the  column  of  blood  in  the 
veins  resting  on  suddenly  closed  tricuspid  valve-segments.  It  is 
important  to  distinguish  venous  pulsation  in  the  neck  from  arterial 
pulsation  in  the  same  situation.  If  the  finger  placed  lightly  on  the 
external  jugular  vein  at  the  root  of  the  neck  obliterates  the  pulsa- 
tion it  is  probably  venous ;  if  it  continues  it  is  probably  arterial. 
Moreover,  if  the  vein  emptied  by  passing  the  finger  lightly  over  the 
vessel  from  below  upwards  is  seen  to  fill  from  below,  the  pulsation  is 
certainly  venous  and  obviously  the  result  of  regurgitation  through 
the  tricuspid  orifice.  Venous  distension  of  the  large  trunks  at  the 
root  of  the  neck  may  also  be  caused  by  chronic  lung  disease,  by 
the  pressure  of  a  tumour  on  the  great  veins  in  the  thorax,  or  by 
tricuspid  stenosis.  Diastohc  collapse  of  the  veins  at  the  root  of 
the  neck  may  occur  in  cases  of  adherent  pericardium.  The  phe- 
nomenon is  supposed  to  depend  on  the  formation  of  fibrous  ad- 
hesions involving  the  great  veins.  Owing  to  the  stretching  of  these 
adhesions  during  the  systole  of  the  ventricles  the  lumen  of  the 
vessels  is  narrowed,  and  thereby  the  onward  flow  of  blood  is 
hindered.  During  diastole,  on  the  other  hand,  the  fibrous  bands 
being  relaxed,  there  is  a  sudden  rush  of  blood  into  the  heart,  conse- 
quent on  the  removal  of  the  obstruction,  and  on  the  suction  power 
of  the  ventricles.     Hence  the  venous  collapse. 

Occasionally  a  pulse  may  be  seen  in  the  peripheral  veins,  such  as 
those  on  the  dorsum  of  the  hand.  The  phenomenon  is  best  seen 
in  cases  of  aortic  regurgitation,  but  may  occur  to  a  slighter  extent  in 
other  conditions. 

Capillary  pulsation. — This  is  observed  in  cases  of  aortic  incompe- 
tence, in  which  the  amount  of  regurgitation  is  considerable  and  the 
power  of  the  left  ventricle  is  still  good. 

A  portion  of  skin,  preferably  of  the  forehead,  should  be  rubbed 
with  the  finger-nail,  or  end  of  the  stethoscope,  and  the  flush  thus 
produced  will  be  seen  to  pulsate  synchronously  with  the  heart's  beat, 
becoming  alternately  red  and  pale.  The  same  appearance  may  often 
be  seen  through  a  thin  slip  of  glass  gently  pressed  on  the  everted 
lip,  or  tip  of  a  finger.  Its  production  depends  on  the  forcible  in- 
jection of  blood  into  the  lax  arterial  system  and  the  sudden  backflow 


METHODS    OF    DIAGNOSIS  33 

into  the  ventricle,  owing  to  the  absence  of  support  to  the  column  of 
blood  by  reason  of  the  incompetence  of  the  aortic  valve. 

Glandular  pidsatio?i. — Occasionally,  as  in  Graves'  disease,  slight 
pulsation  may  be  observed  in  the  thyroid  gland. 

In  some  cases  of  tricuspid  regurgitation  the  whole  liver  may  be 
seen  to  pulsate.  This  phenomenon  is  of  somewhat  rare  occurrence, 
and  is  indicative  of  a  considerable  degree  of  tricuspid  insufficiency. 
Care  must  be  taken  that  transmitted  pulsation  from  the  right 
ventricle  is  not  mistaken  for  true  expansile  pulsation  of  the  organ. 
(See  Palpation.) 

SUB-SECTION  II 

PALPATION 

For  the  purposes  of  palpation  of  the  heart  the  patient  may  be  in 
the  erect  or  recumbent  position,  but  it  is  advisable,  when  possible, 
to  make  use  of  both  postures  in  the  examination. 

The  prsecordium  should  be  palpated  in  the  first  instance  by  the 
whole  hand  placed  flat  upon  the  chest,  and  the  signs  thus  perceived 
may  then  be  localized  by  means  of  one  or  two  fingers.  The  data 
afforded  by  inspection  and  palpation  should  finally  be  compared. 

Palpation  of  the  heart  will  be  considered  under  the  following 
scheme : — 

A.  Pr^cordium 

{a)  The  apex  beat  and  impulse  of  the  left  ventricle 

{b)  The  impulse  of  the  right  ventricle 

{c)  The  auricular  impulse 

(d)  The  diastolic  impulse 

(e)  Closure  of  the  semilunar  valves 

(f)  Vibrations  or  thrills 

1.  Endocardial 

Systolic 

Diastolic 

Presystolic 

2.  Exocardial 

Friction  fremitus 
{g)  Fhictuation 

B.  Great  Vessels 

{a)  Aneurismal  pulsation 
{b)  Diastolic  back  shock 
{c)  Thrills 

1.  Arterial 

2.  Venous 
id)  Tracheal  tugging 

C.  Other  Organs 

D 


34  DISEASES    OF   THE    HEART 

A.   PRiECORDIUM 

(a)  The  Apex  Beat  and  Impulse  of  the  Left  Ventricle 

The  apex  beat  of  the  heart,  which  is  the  expression  of  the  con- 
traction of  the  left  ventricle,  should  be  investigated  with  respect  to 
its  site,  extent,  and  character. 

The  site  of  the  apex  beat.  The  angulus  Ludovici  forms  a  useful 
guide  to  the  level  of  the  second  rib,  immediately  below  which  is  the 
second  intercostal  space,  and  from  this  the  rest  of  the  ribs  and 
spaces  can  be  easily  counted. 

In  adults  the  apex  beat  is  situated  in  the  fifth  intercostal  space 
3^  inches  from  the  mid-sternal  line.  Inability  to  palpate  the  apex 
beat  in  its  normal  situation  may  be  due  to  (a)  the  covering  of  the 
heart  by  lung,  as  in  emphysema ;  ib)  unusual  thickness  of  the  chest 
wall,  depending  on  subcutaneous  fat,  mammary  tissue,  etc. ;  (c)  weak- 
ness of  the  left  ventricle,  and  {d)  displacement  of  the  heart  and 
apex  beat. 

The  heart  and  apex  beat  may  be  displaced  either  from  {a)  in- 
trinsic or  {b)  extrinsic  causes. 

The  intrinsic  causes  of  displacement  of  the  apex  beat  are  hyper- 
trophy or  dilatation  of  the  ventricles,  or,  as  more  commonly 
happens,  a  combination  of  the  two  conditions. 

The  apparent  upward  displacement  of  the  apex  beat  in  peri- 
cardial effusion  is,  in  all  probability,  due  to  the  separation  of  the 
lower  portion  of  the  left  ventricle  from  the  chest  wall  by  a  layer  of 
fluid.  If  the  patient  leans  well  forward,  by  which  means  the 
ventricle  is  brought  nearer  to  the  chest  wall,  the  apex  beat  may 
become  palpable  in  its  normal  situation.  This  manoeuvre  is 
frequently  sufficient  to  render  the  apex  beat  easily  palpable  in  other 
cases  in  which,  under  the  ordinary  conditions  of  examination,  the 
sign  cannot  be  perceived,  or  is  very  indistinct. 

In  hypertrophy  of  the  left  ventricle  the  apex  beat  is  displaced 
downwards  and  slightly  outwards;  in  dilatation  it  is  displaced 
outwards  and  slightly  downwards.  As  a  rule  the  two  causes  of 
displacement  are  variously  combined. 

In  some  instances  of  well-compensated  aortic  stenosis  there 
is  reason  to  believe  that  the  apex  beat  may  not  be  palpable ;  but 
this  point  will  receive  further  consideration  under  the  account  of  the 
valvular  disease  in  question. 

Enlargement  of  the  right  ventricle  displaces  the  apex  beat 
outwards. 

The  extrinsic  causes  of  displacement  of  the  heart  and  apex  beat 
may  be  congenital  or  acquired. 

Congenital  displacement  of  the  heart  will  be  considered  under 
the  head  of  "Malformations  and  Misplacements  of  the  Heart." 

The  acquired  causes  of  displacement  of  the  heart  and  apex  beat 
operate  by  means  either  of  pressure  or  traction  on  the  organ,  which 


METHODS   OF   DIAGNOSIS  35 

may  in  consequence  be  dislocated  towards  the  right  or  left,  up- 
wards or  downwards,  backwards  or  forwards. 

Displacement  of  the  heart  a?td  apex  beat  to  the  right. — This  may  be 
due  to  the  pressure  of  fluid,  gaseous,  or  solid  accumulations  in  the 
left  pleural  cavity,  or  to  extensive  consolidation  of  the  left  lung. 

The  heart  may  be  drawn  towards  the  right  by  retraction  of  the 
right  lung  following  pleural  effusion ;  by  the  contraction  of  pleuro- 
pericardial  adhesions,  of  pulmonary  cirrhosis,  or  of  cavities  in 
phthisis  ;  and  by  collapse  of  the  right  lung  from  pressure  on  the 
main  bronchus  on  the  right  side. 

Displacement  of  the  heart  and  apex  beat  to  the  left. — Dislocation 
of  the  heart  to  the  left  may  depend  on  fluid,  gaseous,  or  solid 
accumulations  in  the  right  pleural  cavity,  or  on  extensive  pneumonic 
consolidation  of  the  right  lung.  It  may  also  be  due  to  contraction 
of  the  left  lung  from  any  of  the  causes  already  enumerated. 
Aneurism  of  the  first  or  second  portion  of  the  arch  of  the  aorta 
is  an  occasional  cause  of  displacement  of  the  apex  beat  to  the  left. 

Displacement  upwards  of  the  heart  and  apex  beat. — This  form  of 
displacement  may  be  caused  by  fluid,  gaseous,  or  solid  collections 
in  the  abdominal  cavity,  such  as  ascites,  tympanites,  tumours  of  the 
liver,  the  pregnant  uterus,  and  abdominal  tumours  of  all  kinds. 
Retraction  of  the  upper  portion  of  either  lung  may  also  give  rise  to 
upward  displacement  of  the  heart. 

Displacement  downtvards  of  the  heart  and  apex  beat. — Hypertroph- 
ous  emphysema  is  the  commonest  cause  of  this  variety  of  cardiac 
displacement,  which  is  very  frequently  observed.  Tumours  at  the 
base  of  the  heart  and  collapse  of  the  abdominal  viscera  also  lead  to 
downward  dislocation  of  the  organ. 

Displacement  backwards  of  the  heart  and  apex  beat. — This  variety 
of  displacement,  which  is  very  rare,  may  be  produced  by  large  peri- 
cardial effusions,  and  by  tumours  or  inflammatory  accumulations  in 
the  anterior  mediastinum. 

Displacement  forwards  of  the  heart  and  apex  beat. — Forward  dis- 
location of  the  heart  is  very  uncommon,  but  it  is  occasionally 
observed  as  the  result  of  the  pressure  of  a  tumour  situated  in  the 
posterior  mediastinum. 

It  will  thus  appear  that  the  determination  of  the  site  of  the  apex 
beat  is  a  point  of  the  greatest  value  in  the  diagnosis,  not  only  of 
diseases  of  the  heart,  but  also  of  the  lungs,  and  it  not  infrequently 
happens  that  the  careful  location  of  this  sign  supplies  the  key  to  the 
elucidation  of  many  obscure  affections  of  the  chest. 

The  extetit  of  the  apex  beat. — The  apex  beat  may  be  localized  or 
diffuse.  Speaking  generally  it  may  be  stated  that  in  hypertrophy  of 
the  left  ventricle  the  apex  beat  is  defined  and  localized,  whereas  in 
dilatation  it  is  hesitant,  uncertain,  and  diffuse.  A  combination  of 
hypertrophy  and  dilatation  often  gives  rise  to  a  wide  area  of  pulsa- 


36  DISEASES    OF   THE    HEART 

tion,  which  occasionally  involves  a  large  portion  of  the  anterior 
surface  of  the  left  chest. 

The  character  of  the  apex  beat. — The  apex  beat  may  convey  the 
sensation  of  a  powerful  prolonged  heave  or  thrust,  or  of  a  short, 
sharp  tap,  or  slap.  The  former  phenomenon  is  indicative  of  hyper- 
trophy, the  latter  of  dilatation  of  the  left  ventricle.  A  typical 
example  of  the  first  condition  is  provided  by  a  fully  compensated 
case  of  aortic  insufficiency,  and  of  the  second,  by  fatty  degeneration 
of  the  heart  wall.  Various  combinations  of  the  two  above-mentioned 
conditions  may  be  observed,  with  corresponding  modifications  in  the 
character  of  the  apex  beat. 

The  importance  of  a  careful  estimation  of  the  character  of  the 
apex  beat  must  be  insisted  on,  since  it  is  a  factor  of  the  first  magni- 
tude in  the  forming  of  a  prognosis  in  valvular  and  myocardial 
diseases  of  the  heart. 

The  effect  of  respiration  and  change  of  posture  on  the  position  of 
the  apex  beat  should  be  carefully  noted  in  all  cases.     • 

{b)  The  Impulse  of  the  Right  Ventricle 

In  cases  of  enlargement  of  the  right  ventricle  the  degree  of  vigour 
of  the  ventricular  contraction  may  be  gauged  by  palpation  in  the 
epigastric  region.  In  disease  at  the  mitral  orifice,  whether  obstruc- 
tive or  regurgitant,  the  task  of  maintaining  the  pulmonary  circulation, 
or  in  other  words  of  providing  compensation,  falls  on  the  right 
ventricle ;  hence  the  importance  of  investigating  the  strength  of  the 
ventricular  impulse. 

The  character  of  the  impulse  would  have  to  be  considered  in  con- 
junction with  the  competency  or  incompetency  of  the  tricuspid 
valve. 

(c)  The  Auricular  Impulse 

Occasionally  it  is  possible,  by  placing  the  tips  of  the  fingers  in  the 
second,  third,  and  fourth  right  intercostal  spaces  close  to  the  sternum, 
to  feel  an  impulse  resulting  from  the  contraction  of  the  right  auricle. 
The  impulse  is  presystolic  in  time.  A  similar  phenomenon  is  said 
to  have  been  observed,  in  children  only,  in  the  corresponding  situa- 
tion on  the  left  side,  and  has  been  ascribed  to  the  contraction  of  the 
left  auricle. 

{d)  The  Diastolic  Impulse 

This  is  very  rarely  observed,  but  ^vhen  present  it  is  felt  as  an 
impulse  during  the  diastole  of  the  ventricles.  It  is  usually  found  in 
association  with  a  variable  degree  of  ventricular  dilatation,  and  with 
a  sudden  sharp  systole  of  the  heart.  It  is  more  commonly  observed 
in  children  than  in  adults.  A  pecuhar  diastolic  shock  or  retraction, 
palpable  over  the  apex  or  right  ventricle,  may  be  due  to  the 
presence  of  pericardial  adhesions. 


METHODS    OF   DIAGNOSIS  37 

{e)  The  Closure  of  the  Semilunar  Valves 

The  closure  of  the  pulmonic  semilunar  valves  may  sometimes  be 
felt  in  those  conditions  in  which,  owing  to  the  retraction  of  the  left 
lung,  the  pulmonary  artery  comes  nearer  to  the  chest  wall.  Under 
these  circumstances  the  artery  is  often  somewhat  dilated.  The 
closure  of  the  aortic  valve  may  also  be  felt  in  cases  of  high  arterial 
tension  with  dilatation  of  the  ascending  portion  of  the  aorta  just 
above  the  sigmoid  cusps. 

{/)  Vibrations  or  Tlxrills 

I.  Endocardial. — The  peculiar  and  characteristic  vibratory  or 
quivering  sensation,  which  may  be  felt  by  the  hand  placed  over  the 
heart,  is  known  as  a  thrill. 

In  the  examination  of  a  thrill  attention  should  be  directed  to  {a) 
its  position  and  {l>)  its  time  relation  with  respect  to  the  cardiac 
cycle,  which  is  determined  by  placing  a  finger  on  the  apex  beat,  or 
carotid  pulse,  while  the  other  hand  palpates  the  thrill. 

A  thrill  that  is  synchronous  with  the  ventricular  impulse  is  called 
systolic,  while  one  that  alternates  with  the  impulse  is  termed 
diastolic.  The  diastolic  thrill  may  be  felt  throughout  the  diastole 
of  the  ventricles,  or  it  may  be  palpable  during  the  early  part  only  of 
the  diastole,  when  it  is  called  an  early  diastolic  or  post-systolic  thrill, 
or  during  the  late  part  only  of  the  diastolic  period,  when  it  is  known 
as  a  late  diastolic  or  presystolic  thrill. 

A  systolic  thrill  felt  over  the  apex  beat  indicates  mitral  incom- 
petence ;  a  presystolic  or  diastolic  thrill  in  this  situation  is  indicative 
of  mitral  obstruction,  but,  as  will  be  shown  later,  it  may  be  asso- 
ciated with  aortic  regurgitation. 

Thrills  felt  over  the  base  of  the  heart;  in  the  second  right  inter- 
costal space  close  to  the  sternal  edge,  or  in  the  episternal  notch,  are 
indicative  of  disease  at  the  aortic  orifice.  If  systolic,  the  opening  is 
obstructed,  if  diastolic,  the  valves  are  incompetent.  DiastoHc  thrills 
due  to  aortic  insufficiency  may  also  be  felt  along  the  right  sternal 
edge  as  low  as  the  fifth  costal  cartilage,  and  in  the  second,  third, 
and  fourth  left  intercostal  spaces  close  to  the  sternum,  as  well  as  at 
the  apex  beat.  Dilatation  of  the  aorta  just  above  the  valve  may 
give  rise  to  a  systolic  thrill  in  the  second  right  interspace. 

Thrills  felt  in  the  second  left  intercostal  space  or  over  the  third 
left  costal  cartilage  close  to  the  edge  of  the  sternum,  indicate  disease 
at  the  pulmonic  opening.  If  systolic,  the  orifice  is  obstructed,  if 
diastolic,  the  valve  is  incompetent. 

A  presystolic  thrill,  palpable  in  the  fourth  and  fifth  intercostal 
spaces  close  to  the  sternum,  or  over  the  xiphoid  cartilage,  is  in- 
dicative of  tricuspid  stenosis. 

Congenital  disease  of  the  heart  not  infrequently  gives  rise  to  a 
prsecordial  thrill,  which  is  more  commonly  felt  over  the  base  of 
the  organ  than  at  the  apex. 

The  intensity  of  a  thrill  is  often  markedly  affected  by  alterations 
in  the  position  of  the  patient. 


38  DISEASES    OF   THE    HEART 

2.  Exocardial.  Friction  fremitus. — This  sign,  which  is  the  result 
of  the  rubbing  together  of  roughened  pericardial  surfaces,  is  generally 
felt  earliest  over  the  base  of  the  heart,  or  over  the  region  of  the  fourth 
left  costal  cartilage.  It  is  commonly  systolic  in  time,  but  it  may 
have  a  double  rhythm,  i.e.  systolic  and  diastolic,  and  gives  the 
sensation  of  a  rubbing  movement  to  the  hand. 

Pleuro-pericardial  friction  fremitus  is  sometimes  felt  in  the  region 
of  the  apex  beat  and  along  the  left  border  of  the  heart  as  high  as  the 
third  rib. 

{£)  Fluctuation 

Fluctuation  is  occasionally  felt  over  the  prsecordial  region  in 
cases  of  long-standing,  large  pericardial  effusion. 

B.    GREAT  VESSELS 

(a)  Aneurismal  Pulsation 

It  has  already  been  stated  that  pulsation  above  the  level  of  the 
third  rib  is  generally  aneurismal.  The  features  to  be  observed  on 
palpation  are  the  rhythm,  which  will  be  systolic,  and  the  character 
of  the  pulsation,  which  will  be  expansile. 

{b)  Diastolic  Back  Shock 

It  has  already  been  mentioned  that  a  diastohc  back  shock  may  be 
felt  over  the  aortic  cartilage  (second  right)  in  cases  of  high  arterial 
tension.  A  similar  phenomenon  may  be  observed  in  aneurismal 
conditions  of  the  aorta. 

{c)  Thrills 

1.  Arterial. — A  thrill,  systolic  or  diastolic  in  time,  may  be  felt 
over  an  aneurism. 

2.  Venous. — A  venous  thrill  may  often  be  felt  in  the  jugular  veins 
at  the  root  of  the  neck  in  cases  of  chlorosis  and  annsmia.  The 
proper  appreciation  of  these  thrills  necessitates  the  gentlest  palpation, 

{d)  Tracheal  Tugging 

This  phenomenon,  which  is  said  to  be  indicative  of  aneurism  of 
the  first  part  of  the  aortic  arch,  is  obtained,  according  to  Dr.  Ewart, 
as  follows :  The  patient  being  seated,  the  operator,  standing  behind 
him,  places  the  tips  of  the  index  fingers  under  the  lower  edge  of  the 
cricoid  cartilage,  and  gently  raises  it.  The  patient's  head  rests  on 
the  chest  of  the  operator.  The  sign  consists  in  a  downward  traction 
of  the  trachea,  felt  with  each  systole  of  the  heart.  It  is  not  present 
in  all  cases  of  aneurism  of  the  first  part  of  the  arch,  nor  is  it  patho- 
gnomonic of  this  condition. 

C.    OTHER   ORGANS 

A  feeble  pulsation  may  sometimes  be  felt  in  the  thyroid  gland 
with  each  systole  of  the  heart. 

Pulsation  of  the  liver  is  best  appreciated  by  means  of  palpation, 
and   its   expansile   character   should   be  carefully   observed.      The 


METHODS   OF   DIAGNOSIS  39 

possibility  of  transmitted  pulsation  from  the  right  heart  should  be 
excluded  before  the  existence  of  true  pulsation  is  admitted. 

The  lower  edge  of  the  liver  is  frequently  palpable  in  cases  of 
hepatic  enlargement. 

Cardiac  disease,  as  Dr.  Head's  brilliant  investigations  have 
shown,  is  attended  by  referred  pain  and  tenderness  over  certain  well 
defined  areas  of  the  chest  and  scalp.  Thus  affections  of  the 
aortic  area  and  ventricle  give  rise  to  reflected  pain  and  tenderness 
over  the  upper  areas  of  the  chest  (2,  3,  4,  5  dorsal)  and  the  mid- 
orbital  region  of  the  scalp.  Lesions  of  the  mitral  area  and  auricles 
are  attended  by  referred  pain  and  tenderness,  in  the  lower  part 
of  the  chest  and  upper  part  of  the  abdomen  (5,  6,  7,  8,  9,  dorsal 
areas)  and  in  the  temporal  and  fronto-temporal  areas  of  the  scalp. 
The  tenderness  in  these  areas  can  be  elicited  by  picking  up  the 
superficial  structures  between  the  thumb  and  finger,  or  by  means  of 
the  blunt  end  of  a  pin. 

SUI3-SECTI0N    III. 
PERCUSSION 

Two  signs  are  elicited  by  means  of  percussion  :  the  first  and 
more  important  being  the  sound  emitted  by  the  part  percussed, 
and  the  second,  the  degree  of  resistance,  or  the  density  of  the 
spot  that  is  struck. 

Percussion  is  distinguished  under  the  terms  'superficial'  or  'deep,' 
according  as  the  finger  or  pleximeter  is  struck  gently  or  forcibly. 

Percussion  of  the  cardiac  area  will  be  considered  under  the 
following  arrangement : — 

A.  Heart 

{a)  Superficial  cardiac  dulness 

1.  Increase  of 

2.  Diminution  of 
(<^)  Deep  cardiac  dulness 

1.  Lateral  increase  of 

2.  Upward  increase  of 

3.  Downward  increase  of 

B.  Pericardium 

{a)  Dulness  dtie  to  effusion 
(l>)  Dulness  due  to  adhesions 

C.  Great  Vessels 

D.  Other  Organs 

A.    HEART 

{a)  Superficial  Cardiac  Dulness 

By  superficial  cardiac  dulness  is  meant  the  extent  of  the  heart's 
surface  which  is  uncovered  by  the  lung,  and  in  contact  with  the 
chest  wall.  This  area  has  already  been  marked  out,  under  normal 
conditions,  on  the  surface  of  the  chest  (see  p.  6),  and  it  is  necessary 
only  to  add  that  light  percussion  should  be  used  in  defining  its 
outline. 


40  DISEASES    OF   THE    HEART 

1.  Increase  of:  The  area  of  superficial  cardiac  dulness  is  in- 
creased by  (a)  deep  expiration,  (i>)  lying  on  the  left  side,  (c)  retraction 
of  the  lungs,  (d)  enlargement  of  the  heart,  and  (e)  pericardial  effusion 
and  pericardial  adhesions. 

2.  Diminution  of:  The  area  of  superficial  cardiac  dulness  is 
diminished  by  (a)  deep  inspiration,  {^)  emphysema,  (c)  pneumo- 
pericardium, (d)  displacement  of  the  heart  due  to  air  in  the  pleural 
cavities,  stomach,  intestine,  and  abdominal  cavity,  or  to  pleuro- 
pericardial  adhesions,  which  may  drag  the  organ  under  the  lungs, 
and  possibly  by  (e)  atrophy  of  the  heart. 

The  information  obtained  by  the  superficial  method  of  cardiac 
percussion  is,  on  the  whole,  more  useful  in  the  diagnosis  of  diseases 
of  the  lungs  than  of  the  heart. 

(d)  Deep  Cardiac  Dulness 

The  area  of  deep  cardiac  dulness  corresponds  approximately 
with  the  size  of  the  heart.  The  outline  of  the  organ  on  the  surface 
of  the  chest  under  normal  conditions  has  already  been  mapped 
out  (see  p.  5)  and  need  not  be  described  again.  In  order  to  trace 
out  the  area  in  question  deep  percussion  should  be  employed  and 
a  definite  mode  of  procedure  adopted. 

Percussion,  in  all  cases,  whether  superficial  or  deep,  should  be 
commenced  well  outside  the  normal  limits  of  the  dulness  to  be 
percussed,  and  the  finger  is  then  gradually  advanced  towards  the  line 
where  resonance  is  impaired.  In  the  case  of  deep  cardiac  dulness, 
for  instance,  the  point  where  the  lung  resonance  begins  to  be 
interfered  with  by  the  underlying  heart  should  be  marked  on  the 
chest  wall,  and  the  joining  of  the  points,  obtained  by  percussion 
from  all  sides,  will  represent  the  outline  of  the  heart. 

I.  Lateral  increase  of  the  area  of  deep  cardiac  dulness. 
Increase  to  the  right :  For  clinical  purposes  the  right  limit  of  cardiac 
dulness,  under  normal  conditions,  is  defined  by  the  right  edge  of 
the  sternum.  Extension  of  dulness  beyond  this  line  means  enlarge- 
ment of  the  right  auricle  and  a  priori  of  the  right  ventricle.  It  will 
be  noticed  that  the  right  limit  of  cardiac  dulness  as  obtained  by 
precussion  does  not  exactly  correspond  with  the  outline  of  the  right 
auricle  as  marked  out  on  the  chest  wall  (see  diagram,  p.  5).  This 
is  due  to  the  fact  that  the  outline  of  the  heart  is  drawn  from 
measurements  in  the  cadaver,  whereas  in  life  it  is  probable  that, 
owing  to  the  pressure  of  the  inflated  right  lung,  and  the  tone  of 
the  auricular  wall,  the  right  auricle  is  situated  rather  more  to  the 
left  than  is  represented. 

Increase  to  the  left :  Extension  of  the  cardiac  dulness  beyond  the 
left  vertical  nipple  line,  which  is  the  normal  limit,  indicates  dilatation 
of  the  left  ventricle. 

Increase  to  the  right  and  left:  A  bilateral  increase  of  the  cardiac 
dulness  is  indicative  of  enlargement  of  both  sides  of  the  heart,  and 
is  the  condition  that  is  commonly  found. 


METHODS   OF   DIAGNOSIS  41 

2.  Upward    increase    of    the    area    of    deep    cardiac    dulness. 

The  upper  limit  of  cardiac  dulness,  under  normal  conditions,  is 
the  level  of  the  third  rib.  Extension  of  dulness  above  this  line 
means,  in  the  absence  of  pericardial  effusion,  enlargement  of  the 
infundibulum  of  the  right  ventricle,  enlargement  of  the  left  auricle, 
aneurism  of  the  aorta  or  mediastinal  tumour. 

3.  Downward  increase  of  the  area  of  deep  cardiac  dulness. 

The  downward  extent  of  cardiac  dulness  is  often  difficult  to  define 
accurately,  owing  to  the  presence  of  the  liver. 

The  lower  limit  of  the  left-sided  portion  of  the  organ  can  gener- 
ally be  made  out,  especially  if  the  stomach  is  distended  with  gas, 
and  the  lower  Hmit  of  the  right- sided  portion  may  often  be  ap- 
proximately determined  by  a  shght  increase  in  the  intensity  of  the 
dulness,  and  a  feeling  of  increased  resistance  on  passing  from  the 
heart  to  the  liver. 

When  the  lower  limit  of  the  heart  cannot  be  determined  by 
percussion,  it  may  be  nearly  defined  by  drawing  a  line,  slightly 
curved  upwards,  from  the  apex  beat  to  the  angle  of  junction  of  the 
upper  limit  of  liver  dulness  with  the  right  limit  of  cardiac  dulness. 

Extension  downwards  of  the  cardiac  dulness  means,  on  the  left  side 
of  the  heart,  hypertrophy  of  the  left  ventricle,  and  on  the  right  side 
of  the  organ,  enlargement  of  the  right  ventricle. 

An  increase  in  the  area  of  cardiac  dulness  downwards  and  to 
the  left  indicates  hypertrophy  and  dilatation  of  the  left  ventricle. 


B.     PERICARDIUM 

{a)  Dulness  due  to  Effusion 

Effusion  into  the  pericardial  cavity  causes  an  increase  upwards 
of  the  praecordial  dulness,  which  may  reach  as  high  as  the  cartilage 
of  the  first  rib.  It  may  extend  downwards  as  low  as  the  sixth  rib 
or  space,  while  laterally  it  may,  with  a  copious  effusion,  stretch  from 
the  right  vertical  nipple  line  to  the  left  axillary  line. 

The  shape  of  the  area  of  dulness  is  pyriform  when  the  amount  of 
effusion  is  slight,  and  pyramidal  or  triangular  when  it  is  extensive, 
with  the  base  of  the  figure  directed  downwards  in  both  cases.  Owing 
to  the  pushing  aside  of  the  lungs  by  the  enlarged  pericardial  sac, 
the  line  of  dulness  separating  it  from  the  pulmonary  tissue  is  abrupt 
and  well  defined,  and  the  finger  experiences  a  sense  of  increased 
resistance  over  the  effusion. 

The  relation  of  the  apex  beat  to  the  area  of  dulness  must  be 
carefully  ascertained. 

With  a  copious  pericardial  effusion  the  apex  beat  lies  well  above 
and  inside  the  area  of  dulness,  that  is  to  say  the  dulness  due  to  the 
effusion  extends  below  and  outside  the  apex  beat. 


42  DISEASES    OF   THE    HEART 

(b)  Dulness  due  to  Adhesions 

Pericardial  adhesions  are  often  associated  with  a  permanent 
increase  in  the  area  of  cardiac  dulness,  which  depends  on  en- 
largement of  the  heart. 

C.     GREAT  VESSELS 

Dulness  due  to  dilatation  of  the  ascending  aorta  may  often  be 
percussed  out  over  the  second  right  intercostal  space  and  adjacent 
portion  of  the  sternum,  and  appears  as  an  extension  upwards  and  to 
the  right  of  the  cardiac  dulness.  Aneurism  of  the  vessel  gives  rise 
to  a  larger  area  of  dulness  in  this  situation. 

Dulness  over  the  upper  sternal  region  and  adjacent  portion  of  the 
left  side  of  the  thorax  is  sometimes  associated  with  aneurism  of 
the  transverse  portion  of  the  aortic  arch. 

Dilatation  of  the  pulmonary  artery  gives  rise  to  dulness  in  the 
second  left  interspace  close  to  the  edge  of  the  sternum. 

D.    OTHER  ORGANS 

The  size  of  the  liver  should  always  be  determined  by  means 
of  palpation  and  percussion  in  cases  of  morbus  cordis.  Normally 
the  upward  extent  of  the  organ  in  the  right  vertical  nipple  line 
is  the  level  of  the  sixth  rib,  though  the  upper  surface  of  the  liver, 
owing  to  its  dome-shaped  conformation,  corresponds,  in  easy  breath- 
ing, with  a  horizontal  line  drawn  at  the  level  of  the  base  of  the 
ensiform  cartilage,  or  middle  of  the  eighth  dorsal  vertebra.  The 
downward  extent  of  the  Hver  in  the  nipple  line  is  the  costal  margin, 
while  in  the  median  line  it  extends  one  and  a  half  inches  below  the 
base  of  the  xiphoid  cartilage. 

Enlargement  of  the  liver  is  one  of  the  earliest  indications  of 
interference  with  passage  of  blood  through  the  right  heart  and 
lungs,  hence  the  importance  of  a  systematic  examination  of  the 
organ  in  all  cases  of  heart  disease.  Indeed,  so  sensitive  is  the 
liver  to  disturbance  of  the  blood  current  through  the  right  heart 
and  lungs  that  it  might  almost  be  called  "  the  barometer  of  the 
circulation." 

SUB-SECTION  IV 

AUSCULTATION 

Auscultation  of  the  heart  will  be  considered  under  the  following 
scheme : — 

A.  Heart  Sounds  and  their  Modifications 
{a)  Position  and  direction  of  cofzdicction 
{b)   Character 
{c)  Rhythm 
{d)  Reduplication 


METHODS   OF   DIAGNOSIS  43 

B.  Adventitious  Sounds 

{a)  Endocardial 

1.  Organic  murmurs 

Physical  causes  of 

Site  of  production  and  direction  of  transmission 

Character 

Rhythm 

2.  H^mic  murmurs 

Causes  of 

Site  of  production  and  direction  of  transmission 

Character 

Rhythm 

ip)  Exocardial 

1.  Friction  sounds 

Pericardial 

Pleural 

Pleuro-pericardial 

2.  Murmurs 

Cardio-pulmonary 

C.  Vascular  Sounds 

1.  Normal  sounds 

2.  Adventitious  sounds 

Arterial 
Venous 

A.   THE   HEART   SOUNDS  AND  THEIR   MODIFICATIONS 

The  normal  sounds. — The  method  of  production  of  the  normal 
sounds  of  the  heart  has  already  been  discussed  (see  p.  12),  and 
does  not  require  any  further  consideration. 

Before  describing  the  position  in  which  the  sounds  are  heard, 
a  brief  account  will  be  given  of  the  mode  of  procedure  that  should 
be  adopted  in  auscultating  the  heart. 

The  chest  piece  of  the  stethoscope  is  placed  firstly  over  the  apex 
beat  and  the  region  of  the  chest  wall  immediately  surrounding  it, 
which  may  collectively  be  termed  the  '"mitral  area."  The  instru- 
ment is  then  gradually  advanced,  obliquely  upwards  and  outwards, 
into  the  left  axilla,  and  thence  as  far  as  the  angle  of  the  left  scapula. 
It  is  then  placed  upon  successive  points  on  the  chest  wall,  in  a 
line  connecting  the  apex  beat  with  the  second  right  costal  cartilage, 
at  its  junction  with  the  sternum.  The  second  right  costal  cartilage 
is  known  as  the  "  aortic  cartilage,"  and  this  region  of  the  chest  wall, 
with  the  adjacent  portion  of  the  second  interspace,  is  called  the 
"aortic  area."  From  here  the  stethoscope  is  carried  upwards  to  the 
episternal  notch  and  right  side  of  the  neck  over  the  carotid  artery, 


44  DISEASES   OF   THE  HEART 

and  downwards  along  the  right  sternal  edge.  It  is  then  placed 
close  to  the  sternum  over  the  second  left  costal  cartilage,  ternaed 
the  "pulmonary  cartilage,"  which  with  the  adjacent  portion  of 
the  second  interspace  is  known  as  the  "pulmonary  area."  The 
instrument  is  now  carried  along  the  left  sternal  edge  to  the  base 
of  the  ensiform  cartilage.  The  fourth  and  fifth  left  intercostal 
spaces,  for  about  an  inch  to  the  left  of  the  sternum,  and  the  region 
of  the  chest  wall  immediately  surrounding  the  base  of  the  ensiform 
cartilage,  are  collectively  termed  the  "  tricuspid  area." 


FIG.    6.      THE   AREAS    IN   WHICH   THE   SOUNDS    PRODUCED   AT   THE   VARIOUS 
CARDIAC   ORIFICES   ARE    MOST    DISTINCTLY    HEARD 

M  (within  circle)  =  mitral  area  ;  A  (within  circle)  =  aortic  area  ;  T  (within  circle)  =  tricuspid  area 
P  (within  circle)  =  pulmonary  area 

To  distinguish  between  the  two  sounds  of  the  heart,  a  finger 
should  be  put  on  the  apex  beat,  or  on  the  carotid  artery  in  the 
neck,  while  the  stethoscope  is  placed  in  the  mitral  area;  the  first 
sound  is  synchronous  with  the  cardiac  impulse  or  pulse  wave,  as 
the  case  may  be. 


METHODS    OF   DIAGNOSIS  45 

{a)  Position  and  Direction  of  Conduction  of  the  Normal 
Heart  Sounds 

The  left  ventricle  first  sound. — The  left  ventricle  first  sound  is 
most  distinctly  audible  at  and  to  the  left  of  the  apex  beat.  It  is 
also  heard  with  a  variable  degree  of  distinctness  in  the  aortic  area. 

The  aortic  second  sound.- — -The  aortic  second  sound  is  heard  best 
in  the  aortic  area,  but  it  is  distinctly  audible  over  the  carotid  arteries 
in  the  neck,  especially  on  the  right  side,  and  in  this  situation  is  not 
liable  to  be  confused  with  the  pulmonic  second  sound.  The  aortic 
second  sound  can  also  be  well  heard  at  and  to  the  left  of  the  apex 
beat. 

The  puiniofiic  second  sound.— The.  pulmonic  second  sound  is  heard 
most  distinctly  in  the  second  left  interspace  close  to  the  sternum. 
It  is  also  plainly  audible  over  the  second  left  costal  cartilage,  and 
over  the  whole  of  the  right  ventricle.  It  is  not  normally  audible  at 
the  apex  of  the  heart. 

The  right  ventricle  first  sound.  —  The  first  sound  of  the  right 
ventricle  is  heard  over  the  whole  of  the  organ  in  relation  with  the 
chest  wall,  but  it  is  most  distinctly  audible  in  the  tricuspid  area. 

It  will  be  noticed  that  the  areas  in  which  the  various  heart  sounds 
are  best  heard  do  not  necessarily  correspond  with  the  anatomical  posi- 
tion of  the  structures  producing  them,  and  for  the  following  reasons. 

It  has  already  been  explained  that  the  first  sound  of  the  heart  is 
composed  of  a  muscular  and  a  valvular  element.  The  muscular 
element  of  the  first  sound  gives  rise  to  no  difficulty,  as  it  is  naturally 
heard  most  distinctly  where  the  ventricles  are  in  closest  contact  with 
the  chest  wall,  and  hence,  in  the  case  of  the  left  ventricle,  is  most 
plainly  audible  at  the  apex  of  the  heart. 

The  valvular  element  of  the  first  sound  of  the  left  ventricle  is  not 
audible  over  the  anatomical  position  of  the  mitral  orifice,  because 
here  a  considerable  thickness  of  lung  tissue,  which  is  a  bad  con- 
ductor of  sound,  is  interposed  between  the  heart  and  chest  wall. 
The  valvular  vibrations  are,  however,  transmitted  along  the  wall  of 
the  left  ventricle,  and  are  best  heard  at  the  apex  of  the  heart,  which, 
uncovered  by  lung,  comes  into  close  relation  with  the  thoracic  parietes. 

For  similar  reasons  the  first  sound  of  the  right  ventricle  is  most 
distinctly  audible  in  the  tricuspid  area,  and  not  directly  over  the  site 
of  the  tricuspid  valve.  The  left  ventricle  first  sound  is  heard  in  the 
aortic  area,  and  is  conducted  thither  by  the  walls  of  the  aorta. 

With  respect  to  the  aortic  second  sound,  it  is  heard  most  distinctly 
in  the  aortic  area,  where  the  vessel  comes  nearest  to  the  surface. 
The  vibrations  due  to  the  sudden  tension  of  the  semilunar  valves 
are  transmitted  along  the  course  of  the  aorta  by  means  of  the 
arterial  wall  and  the  contained  column  of  blood.  A  similar 
mechanism  explains  the  conduction  of  the  aortic  second  sound 
into  the  neck,  and  it  is  transmitted  to  the  apex  of  the  heart  by  the 
wall  of  the  left  ventricle. 


46  DISEASES    OF   THE    HEART 

The  reason  that  it  is  not  heard  over  the  site  of  the  aortic  orifice 
is  that  here  the  vessel  is  covered,  not  only  by  lung,  but  also  by  the 
infundibulum  of  the  right  ventricle,  which  interferes  with  the  trans- 
mission of  vibrations  to  the  surface  of  the  chest. 

The  pulmonary  second  sound  is  heard  most  distinctly  over  the 
exact  anatomical  position  of  the  orifice,  viz.  at  the  upper  border  of 
the  third  left  costal  cartilage  close  to  the  sternum.  The  sound  is 
transmitted  upwards  along  the  course  of  the  vessel,  as  high  as  the 
second  costal  cartilage,  and  downwards  by  the  wall  of  the  right 
ventricle,  to  the  base  of  the  ensiform  cartilage,  and  to  within  an 
inch  of  the  apex  beat. 

{b)  Character  of  the  Normal  Sounds  of  the  Heart 

The  sounds  of  the  heart  are  usually  represented  by  the  familiar 
syllables  "  lubb-dup,"  which  correspond  to  the  first  and  second  sounds 
respectively.  They  convey  the  idea  of  sudden  tension,  and  can  be 
imitated  by  the  more  or  less  rapid  stretching  of  longer  and  shorter 
pieces  of  string  or  membrane.  The  border  of  an  ordinary  pocket- 
handkerchief  answers  the  purpose  perfectly  well. 

The  first  sound  is  duller,  longer,  and  louder  than  the  second, 
which  is  short  and  sharp.  Normally  the  left  ventricle  first  sound  is 
duller  and  longer  than  that  of  the  right,  which  is  relatively  short  and 
sharp.  This  difference  is  in  all  probability  explained  by  the  relative 
preponderance  of  the  muscular  element  in  the  production  of  the  left 
ventricle  first  sound. 

The  pulmonary  second  sound  at  the  base  of  the  heart  is  under 
normal  conditions  louder  than  the  aortic,  but,  according  to  some 
observers,  this  statement  is  open  to  doubt.  The  relative  intensity  of 
the  two  sounds  is  apparently  determmed  largely  by  the  age  of  the 
individual  (Cabot). 

{c)  Rhythm  of  the  Normal  Sounds  of  the  Heart 

The  relative  time  duration  of  the  events  composing  the  cardiac 
cycle  may  be  stated  approximately  as  follows  : — . 

The  first  sound  occupies  nearly  three-tenths  of  a  second.  The  in- 
terval between  the  first  and  second  sounds  one-twentieth  of  a  second. 

The  second  sound  occupies  one-tenth  of  a  second.  The  long 
silence,  or  in  other. words  the  diastole  of  the  ventricles,  occupies 
five-tenths  of  a  second. 

Under  normal  conditions  the  relative  lengths  of  the  interval 
between  the  first  and  second  sounds,  and  second  and  first,  are 
preserved,  though  the  rate  of  the  heart  beats  per  minute  may  vary 
within  very  wide  limits. 

Position  and  direction  of  conduction. — In  order  to  avoid  subse- 
quent repetition,  it  may  be  stated  generally  that  the  degree  of 
distinctness  with  which  the  sounds  of  the  heart  are  heard  depends 
not  only  on  the  character  of  the  sound,  but  also  on  the  thickness  of 
the  thoracic  wall,  and  the  extent  to  which  the  organ  is  overlapped 


METHODS   OF   DIAGNOSIS  47 

by  lung  tissue,  or  by  other  material,  such  as  air,  fluid,  solid  tumours, 
etc.  For  example,  the  first  sound  of  the  heart  is  more  or  less 
indistinct  in  cases  of  emphysema  of  the  lungs,  and  of  pericardial 
effusion  or  growths. 

On  the  other  hand,  the  sounds  of  the  heart  become  more  distinct 
in  those  conditions  in  which  the  organ  comes  nearer  to  the  chest 
wall,  as  in  retraction  of  the  lungs,  etc.  Thus  the  pulmonary  second 
sound  may  appear  to  be  accentuated  in  retraction  of  the  left  lung, 
and  similar  effects  are  observed  as  regards  the  other  sounds  of  the 
heart,  under  like  circumstances. 

These  conditions  are  mentioned  in  order  that  due  allowance  may 
be  made  for  them  in  estimating  the  character  of  the  various  cardiac 
sounds. 

The  left  ventricle  first  sound. — In  hypertrophy  of  the  left  ventricle, 
and  in  cases  of  high  systemic  tension,  the  first  sound  of  the  heart 
becomes  less  distinct,  and  may  be  quite  inaudible  in  the  aortic 
area. 

On  the  other  hand,  it  becomes  more  distinct  in  this  situation,  in 
conditions  of  low  arterial  tension  and  in  dilatation  of  the  left 
ventricle.  Apparently  the  character  of  the  left  ventricle  first  sound 
largely  influences  the  degree  of  its  conduction  along  the  aorta. 

The  aortic  secofid  sound. — The  aortic  second  sound  becomes  in- 
audible at  and  to  the  left  of  the  apex  beat,  when,  owing  to  enlarge- 
ment of  the  right  heart,  the  left  ventricle,  and  with  it  the  apex, 
is  displaced  from  its  normal  position.  This  occurs  in  cases  of 
mitral  stenosis,  though  probably  in  this  disease  the  weakness  of  the 
second  sound  also  affects  its  conduction. 

The  absence  of  the  aortic  second  sound  over  the  carotid  arteries 
in  the  neck  depends  on  damage  to  the  semilunar  valves,  the  result 
of  injury  or  disease,  whereby  these  structures  are  unable  to  offer 
sufficient  check  to  the  backflow  of  blood  towards  the  ventricle  to 
produce  vibrations  of  the  aortic  walls. 

It  will  be  seen,  therefore,  that  the  absence  of  the  second  sound 
in  the  neck  is  indicative  of  a  considerable  amount  of  regurgitation 
into  the  left  ventricle. 

The  pulmonic  second  sound. — This  sound,  in  cases  of  enlargement 
of  the  right  heart,  may  be  heard  as  far  to  the  left  as  the  normal 
position  of  the  apex  beat,  and  is  transmitted  there  by  the  walls  of 
the  right  ventricle,  which  has  usurped  the  place  of  the  left. 

In  some  instances  of  consohdation  of  the  left  upper  lobe  of  the 
lung,  the  pulmonary  second  sound  may  be  heard  over  a  large  area  of 
the  left  chest. 

The  right  vejttricle  first  sound. — In  cases  of  enlargement  of  the 
right  ventricle,  the  first  sound  may  be  heard  further  to  the  left  than 
usual. 


48  DISEASES    OF   THE    HEART 

Modifications  in  the  character  of  the  sounds  of  the  heart. — Three 
distinct  elements  are  to  be  distinguished  in  every  tone,  viz. : — 

1.  Intensity  (loudness) 

2.  Pitch 

3.  Quality  (timbre) 

The  three  elements  taken  together  determine  the  character  of 
a  tone.  With  regard  to  the  sounds  of  the  heart,  which  are  not  true 
musical  tones,  it  is  often  difficult  to  state  with  precision  the  exact 
modifications  that  they  may  undergo.  This  statement  applies  more 
particularly  to  changes  in  quality,  but  the  attempt  will  be  made  to 
state,  so  far  as  possible,  in  technical  language  the  variations  to  which 
the  different  sounds  of  the  heart  are  liable. 

Left  ventricle  first  sound. — Under  normal  conditions  the  variations 
in  character  of  the  left  ventricle  first  sound  are  comparatively  unim- 
portant, and  consist  mainly  in  alterations  in  duration  and  intensity. 

The  first  sound  is  short  and  loud  when  the  ventricle  is  acting 
rapidly  and  the  arterial  tension  is  low,  as  may  occur  in  nervous 
conditions,  for  instance  in  Graves'  disease,  or  in  the  early  stages  of 
fever. 

Conversely,  it  is  long  and  diminished  in  intensity  when  the 
ventricle  is  contracting  slowly  against  increased  systemic  tension. 

In  hypertrophy  of  the  ventricle  the  muscular  element  becomes 
obtrusive,  and  the  first  sound  is  therefore  prolonged  and  dull. 
Stated  in  technical  language,  the  sound  is  characterised  by  increased 
duration,  diminished  intensity,  and  slightly  altered  quality. 

In  dilatation  of  the  ventricle  the  condition  of  affairs  is  reversed. 
Here  the  valvular  element  becomes  prominent,  and  the  sound  is 
short,  sharp,  and  loud.  In  other  words,  the  sound  is  characterised 
by  diminished  duration,  by  heightened  pitch,  and  by  increased  in- 
tensity. The  quality  of  the  sound  also  undergoes  slight  modification 
by  reason  of  the  change  in  the  mechanism  of  its  production. 

Shortness  of  the  left  ventricle  first  sound,  with  diminution  of 
intensity,  which  may  go  on  to  complete  extinction,  is  indicative 
of  extreme  weakness  of  the  ventricular  walls,  and  occurs  in  pro- 
longed febrile  conditions,  such  as  enteric  fever  and  in  other  diseases 
productive  of  protracted  malnutrition  of  the  myocardium. 

In  mitral  stenosis  the  first  sound  of  the  left  ventricle  is  remark- 
ably and  characteristically  short,  sharp,  and  loud,  and  at  the  same 
time  altered  in  quality.  In  cases  of  mitral  regurgitation,  the  first 
sound  may  be  partially  or  wholly  replaced  by  the  systolic  murmur. 

The  aortic  second  sound. — The  most  common  variation  affecting 
this  sound  is  a  change  in  intensity,  which  becomes  either  relatively 
or  absolutely  increased  or  diminished. 

An  increase  in  the  intensity  of  the  sound  produced  at  the  aortic 
or  pulmonic  orifices  is  known  under  the  name  of  accentuation. 

Accentuation  of  the  aortic  second  sound  occurs  in  high  arterial 
tension  with  a  forcibly  acting  left  ventricle.     It  may  also  occur  in 


METHODS    OF   DIAGNOSIS  49 

association  with  low  arterial  tension,  if  the  ventricular  systole  is 
vehement;  but  in  such  cases  the  accentuation  is  not  relatively 
apparent,  owing  to  the  concurrent  accentuation  of  the  pulmonic 
second  sound. 

Accentuation  of  the  aortic  second  sound  is  almost  invariably  pro- 
duced by  dilatation  or  aneurism  of  the  ascending  aorta,  and  in  such 
conditions  the  sound  is  not  only  accentuated  but  is  also  of  markedly 
lower  pitch. 

A  further  modification  of  the  second  sound  is  observed  when, 
in  association  with  dilatation  of  the  vessel,  the  walls  of  the  aorta 
have  undergone  thinning,  and  more  or  less  fusion  of  the  three  coats 
of  the  artery  has  taken  place.  In  addition  to  an  alteration  in 
intensity  and  pitch,  the  sound  now  acquires  a  change  of  quality  to 
a  more  musical  tone,  which  is  highly  characteristic  of  the  affection 
in  question,  though  a  similar  modification  may  be  produced  by 
aneurism  of  one  of  the  sinuses  of  Valsalva. 

Diminution  in  intensity,  or  feebleness  of  the  aortic  second  sound, 
is  associated  with  weakness  of  the  left  ventricle  due  to  myocardial 
inflammation  or  degeneration.  The  second  sound  is  enfeebled  also 
in  mitral  stenosis  and  in  nearly  all  forms  of  disease  affecting  the 
aortic  valve. 

Weakness  or  disappearance  of  the  aortic  second  sound  in  the 
neck  in  cases  of  aortic  incompetence  is  significant  of  a  considerable 
amount  of  valvular  insufficiency. 

The  pulmonic  second  soiuid. — The  pulmonic  second  sound  is 
accentuated  in  all  conditions  which  give  rise  to  obstruction  to  the 
passage  of  blood  through  the  lungs.  It  occurs  therefore  in  affec- 
tions of  the  lungs  such  as  pneumonia,  bronchitis,  emphysema, 
pleural  eifusion,  etc.,  and  sooner  or  later  in  all  diseases  of  the  left 
side  of  the  heart. 

Weakness  of  the  pulmonic  second  sound  is  of  importance  only 
when  observed  in  conjunction  with  previous  accentuation.  With 
this  sequence  of  events,  enfeeblement  of  the  sound  is  indicative  of 
dilatation  of  the  right  ventricle  with  leakage  through  the  tricuspid 
valve. 

The  right  ventricle  first  sound. — So  long  as  the  myocardium 
remains  healthy,  the  right  ventricle  first  sound  is  intensified  in  all 
conditions  which  interfere  with  the  normal  circulation  of  blood 
through  the  lungs.  The  circumstances  under  which  pulmonary 
obstruction  occurs  have  been  referred  to  under  the  causes  of 
accentuation  of  the  pulmonic  second  sound. 

Enfeeblement  of  the  right  heart  first  sound  occurs  as  the  result  of 
myocardial  inflammation  or  degeneration,  and  in  the  later  stages 
of  dilatation  of  the  ventricle  from  any  cause. 


50  DISEASES    OF   THE    HEART 

Modifications  in  the  rhythm  of  the  sounds  of  the  heart. — For 

clinical  purposes  alterations  in  the  relative  time  duration  of  the 
various  events  composing  the  cardiac  cycle  may  be  considered  to 
take  place  in  two  directions,  with  the  result  that  the  sounds  of  the 
heart  are  spaced  (that  is,  separated  by  a  longer  interval  than  normal) 
or  approximated. 

The  first  effect  may  be  produced  either  by  prolongation  of  the 
interval  between  the  first  and  second  sounds,  or  by  the  shortening 
of  the  diastole :  the  second,  by  the  shortening  of  the  interval 
between  the  first  and  second  sounds,  or  by  prolongation  of  the 
diastole. 

Spacing  of  the  sounds  of  the  heart  may  be  carried  to  the  point 
at  which  they  become  equidistant,  and  this  condition  has  been 
termed  embryocardia,  or  the  tick-tack  action  of  the  heart,  from 
its  resemblance  to  the  rhythm  of  the  foetal  heart  sounds,  or  to 
the  ticking  of  the  pendulum  of  a  clock,  or  of  a  watch. 

Equidistance  of  the  two  sounds  of  the  heart,  from  prolongation 
of  the  interval  between  them,  is  found  most  commonly  in  associa- 
tion with  high  arterial  tension,  and  is  then  indicative  of  impending 
failure  of  the  left  ventricle. 

Thus,  in  these  cases,  the  ventricle,  in  spite  of  the  increased 
resistance  to  the  discharge  of  its  contents,  is  still  just  able  to 
empty  itself,  but  it  does  so  with  much  greater  difficulty,  and 
therefore  more  slowly  than  usual ;  hence  the  spacing  of  the 
sounds. 

A  similar  phenomenon  may  be  observed  in  enteric  fever  as  the 
result  of  myocardial  degeneration,  and  is  then  usually  of  fatal 
import. 

Equidistance  of  the  sounds  of  the  heart  is  sometimes  associated 
with  tachycardia,  and  in  such  instances  is  produced  by  the  shortening 
of  the  diastole. 

Approximation  of  the  first  and  second  sounds  of  the  heart  usually 
indicates  weakness  of  the  left  ventricle,  consequent  on  myocardial 
disease,  or  high  arterial  tension.  Here  the  ventricle  does  not  com- 
plete its  contraction  by  reason  of  the  absolute  or  relative  inability 
of  its  muscular  walls  to  maintain  the  intra-ventricular  pressure  above 
that  in  the  aorta  throughout  the  systole.  So  soon,  therefore,  as  the 
pressure  in  the  aorta  exceeds  that  in  the  ventricle  the  semilunar 
valves  close,  and  the  second  sound  occurs.  This  event  may  take 
place  at  any  stage  of  the  ventricular  contraction,  with  a  correspond- 
ing variation  in  the  degree  of  approximation  of  the  sounds.  In 
some  instances  the  second  sound  follows  the  first  almost  im- 
mediately. The  phenomenon  is  observed  vnth  failure  of  the  heart 
in  diphtheria  and  other  acute  febrile  conditions,  and  in  the  early 
and  late  stages  of  kidney  disease.  The  approximation  of  the  sounds, 
under  these  circumstances,  is  of  very  grave  significance. 

Approximation  of  the  sounds  of  the  heart  may  also  be  heard  in 
some  cases  of  low  arterial  tension  with  a  rapid  action  of  the  organ, 


METHODS    OF   DIAGNOSIS  51 

such  as  occurs  in  febrile  and  emotional  states,  and  is  then  of  no 
prognostic  value. 

{d)  Reduplication  of  the  Sounds  of  the  Heart 

Either  the  first  or  second  sound  of  the  heart  may  be  reduplicated. 
The  reduplication  usually  implicates  one  sound  at  a  time,  but 
occasionally  both  are  affected  together.  The  two  elements  com- 
posing the  double  sound  may  be  closely  approximated,  or  they 
may  be  separated  by  an  appreciable  interval,  producing,  in  the 
first  event,  an  effect  resembling  the  double  beat  upon  a  drum, 
and  hence  called  the  "Bruit  de  rappel,"  and  in  the  second,  a 
hkeness  to  the  footfall  of  a  horse  at  a  canter,  the  "  Bruit  de  galop." 

Thus  in  the  case  of  the  doubling  of  the  first  sound  of  the  heart 
the  result  is  heard  as  "lurrub-dup"  or  "  lublub-dup,"  and  of  the 
second,  as  "lub-durrup"  or  "  lub-dupdup,"  according  to  the  degree 
of  separation  of  the  two  elements  of  the  double  sound. 

There  is  no  kind  of  agreement  among  writers  on  the  subject, 
either  as  to  the  cause,  significance,  or  even  area  of  greatest  audibility 
of  the  phenomena  in  question,  and  it  will  be  possible  to  give  but 
a  brief  outline  of  the  views  which  have  been  advanced  to  explain 
them. 

Reduplication  of  the  first  sound  of  the  heart. — Reduplication  of 
the  first  sound  is  usually  most  distinctly  audible  just  internal  to  the 
apex  beat,  and  along  the  line  of  the  interventricular  septum,  but  it 
may  also  be  heard  in  the  tricuspid  area,  and  along  the  left  edge 
of  the  sternum  as  high  as  the  third  rib.  It  is  rarely,  if  ever,  well 
heard  over  the  base  of  the  heart. 

Reduplication  of  the  first  sound  occurs  most  commonly  in 
association  with  hypertrophy  of  the  heart,  the  result  of  high  arterial 
tension,  such  as  obtains  in  some  forms  of  kidney  disease  and  in 
other  disorders. 

It  is  also  observed  in  cases  of  dilatation  of  the  heart  following 
myocardial  disease,  or  pericardial  adhesion,  and  it  may  occur  in  the 
absence  of  any  appreciable  cardiac  lesion  (Potain). 

Reduplication  of  the  first  sound  is  probably  of  little  or  no  clinical 
significance,  except  when  it  is  found  in  association  with  high  arterial 
tension,  particularly  of  nephritic  origin,  and  it  is  then  a  sign  of 
commencing  dilatation  of  the  left  ventricle  from  failure. 

The  doubling  of  the  first  sound  of  the  heart  has  been  ascribed 
to  a  want  of  synchronism  in  the  contraction  of  the  two  ventricles. 
Under  normal  conditions  the  relation  between  the  intra-ventricular 
pressure  and  the  muscular  power  of  the  ventricles  is  so  adjusted 
that  the  two  sides  of  the  heart  contract  simultaneously.  It  is  sup- 
posed that  an  increase  of  intra-ventricular  pressure  occurring  on 
either  side  of  the  heart  might,  if  sufficiently  great,  upset  the 
normal  balance  and  cause  asynchronism.     Thus  the  ventricle  work- 


52  DISEASES    OF   THE    HEART 

ing  against  the  increased  pressure  might  contract  later  (according 
to  Dr.  Barr  earUer)  than  usual,  and  especially  may  this  be  the 
case  if,  as  Sir  William  Broadbent  supposes,  the  ventricle  affected 
is  beginning  to  dilate  before  the  resistance  that  has  to  be  over- 
come. 

Against  this  view  has  been  advanced  the  fact  that  physiologists 
have  never  observed  asynchronism  in  the  contraction  of  the  right 
and  left  sides  of  the  heart.  It  is,  however,  extremely  likely  that 
under  physiological  conditions  of  the  circulation  this  observation 
may  hold  good,  but  it  is  no  argument  against  the  view  that 
asynchronism   might  occur  under  pathological  influences. 

The  reduplication  of  the  sound  is  most  distinctly  audible  along 
the  course  of  the  interventricular  septum,  and  in  some  instances 
is  palpable  in  this  situation.  Moreover,  in  cases  where  doubling 
of  the  first  sound  is  observed,  the  two  elements  composing  it  can 
be  heard  when  the  cusps  of  a  differential  stethoscope  are  placed 
over  the  right  and  left  ventricles,  where  on  separate  examination, 
but  one  sound  is  audible  (Broadbent).  It  would  therefore  appear 
highly  probable  that  a  want  of  synchronism  in  the  contraction  of 
the  two  ventricles  is  a  cause  of  reduplication  of  the  first  sound 
of  the  heart. 

The  explanation  that  has  Just  been  given  may  not,  however,  cover 
all  the  cases  in  which  reduplication  of  the  first  sound  of  the  heart 
is  heard.  The  phenomenon  was  ascribed  by  Dr.  G.  Johnson  to 
an  audible  contraction  of  the  auricle  immediately  preceding  the 
ventricular  systole.  It  is  a  priori  improbable  that  the  auricular 
contraction  could  give  rise  to  a  sound,  and  further,  the  area  of 
audibility  of  the  double  sound  as  described  by  Dr.  Johnson,  and 
on  which  his  view  was  largely  based,  is  contrary  to  the  experience 
of  most  observers. 

Dr.  Sansom  attributes  all  forms  of  reduplication  of  the  sounds  of 
the  heart  to  tension  of  the  curtains  of  left  auriculo-ventricular  valve 
during  some  part  of  the  diastole  of  the  ventricle.  Thus,  in  the  present 
instance,  he  supposes  that  a  forcible  auricular  contraction  causes 
an  impulse  to  the  apex  of  the  left  ventricle,  which  by  contre-coup 
gives  rise  to  vibrations  of  the  mitral  curtains,  and  the  sound  thereby 
produced  is  heard  just  before  the  ventricular  first  sound. 

There  is,  however,  no  cause  in  most  of  the  cases  in  which 
reduplication  of  the  first  sound  occurs  for  a  forcible  contraction 
of  the  auricle,  since  the  stress  of  the  circulation  falls  on  the 
ventricle ;  hence  the  explanation  given  by  Dr.  Sansom  cannot  be 
regarded  as  of  general  application. 

Reduplication  of  the  second  sound  of  the  heart. — Reduplication 
of  the  second  sound  is  usually  most  distinctly  heard  over  the  base 
of  the  heart,  and  at  the  left  edge  of  the  sternum  about  the  level  of 
the  third  intercostal  space.  According  to  Dr.  Sansom  it  is  most 
plainly  audible  just  inside  the  apex  beat,  and  along  the  left  edge 


METHODS    OF   DIAGNOSIS  53 

of  the  sternum,  at  the  level  of  the  junction  of  the  fourth  and  fifth 
costal  cartilages.  There  is  no  doubt  that  an  apparent  doubling 
of  the  second  sound  of  the  heart  is  sometimes  audible  immediately 
to  the  inner  side  of  the  apex  beat  and  not  at  the  base,  in  cases  in 
which  a  presystolic  murmur  subsequently  appears,  but  the  mechanism 
of  its  production  differs  from  that  of  the  reduplication  previously 
mentioned. 

Reduplication  of  the  second  sound  of  the  heart  occurs  most 
commonly  in  mitral  stenosis,  but  it  may  be  observed  with  pul- 
monary obstruction  from  any  cause.  It  is  also  heard  in  pericarditis 
and  myocarditis,  and  in  high  arterial  tension  with  hypertrophy  of 
the  left  ventricle. 

Except  when  it  is  heard  at  the  apex  of  the  heart  and  not  at  the 
base,  reduplication  of  the  second  sound  is  of  no  clinical  significance. 
It  has  been  ascribed  to  a  want  of  synchronism  in  the  closure  of 
the  semilunar  valves  on  the  two  sides  of  the  heart.  The  asyn- 
chronism  may  be  caused  by  increased  systemic  or  pulmonic  tension, 
which  delays  the  completion  of  the  systole  of  the  corresponding 
ventricle,  and  consequently  the  closure  of  the  semilunar  valves. 

This  explanation,  while  accounting  for  the  reduplication  of  the 
second  sound  as  heard  at  the  base  of  the  heart,  does  not  elucidate 
the  apparent  doubling  of  the  second  sound  audible  at  the  apex 
only. 

This  is  probably  due,  as  Dr.  Sansom  suggests,  to  tension  of  the 
segments  of  the  left  auriculo-ventricular  valve,  which  is  caused  by 
a  more  rapid  flow  of  blood  than  usual  into  the  ventricle  during 
the  early  part  of  the  diastole  consequent  on  increased  pressure  in 
the  auricle. 

Apparent  doubling  of  the  second  sound  which  is  heard  in  the 
neighbourhood  of  the  apex  beat  only  is,  therefore,  a  sign  of  con- 
siderable diagnostic  importance,  since  it  is  almost  invariably  the 
precursor  of  a  presystolic  murmur,  indicative  of  stenosis  at  the 
mitral  orifice. 

B.    ADVENTITIOUS  SOUNDS 

{a)  Endocardial 

•  Audible  vibrations,  exclusive  of  the  normal  heart  sounds  and  their 
modifications,  accompanying  the  cardiac  movements,  and  generated 
as  the  result  of  morbid  conditions  of  the  heart  and  pericardium,  are 
known  as  murmurs. 

Such  superadded  or  adventitious  sounds  may  partially  or  wholly 
replace  the  normal  sounds  of  the  heart. 

For  clinical  purposes  murmurs  may  be  divided  into — • 
{ci)  Endocardial  murmurs 
{b)  Exocardial  murmurs 
{c)  Vascular  murmurs 


54  DISEASES   OF   THE    HEART 

Endocardial  murmurs  may  be  further  subdivided  into— 
(a)  Organic  murmurs 
(d)  Functional  or  Haemic  murmurs 

I.  Organic  murmurs. — A  murmur  which  is  due  to  the  presence  of 
an  appreciable  morbid  lesion  is  known  as  an  organic  murmur. 

Physical  Causes  of  Organic  Murmurs 

A  murmur  is  the  sound  produced,  under  certain  conditions,  by 
the  passage  of  gas  or  fluid  along  a  tulDe.  So  long  as  the  tube  has  a 
smooth  internal  surface,  and  does  not  alter  in  calibre,  the  circulation 
of  fluid  through  it  does  not  give  rise  to  any  audible  vibrations.  If, 
however,  a  constriction  be  introduced  at  any  point  along  the  course 
of  the  tube  a  "fluid  vein"  is  formed  immediately  beyond  the  nar- 
rowed portion,  which  gives  rise  to  sonorous  vibrations  that  may  be 
heard  as  a  murmur.  In  the  case  of  the  heart  the  size  of  the  various 
cavities  and  orifices  is  so  adjusted  that,  under  normal  conditions, 
no  sound  is  produced  by  the  circulation  of  blood  through  them. 
Whenever  a  cavity  or  orifice  is  increased  or  diminished  in  size, 
either  relatively  or  absolutely,  the  conditions  for  the  production 
of  a  fluid  vein  are  present,  and  consequently  a  murmur  may  be 
heard. 

So  far  as  the  clinical  expression  of  a  murmur  is  concerned,  it  must 
be  borne  in  mind  that  the  vibrations  in  the  blood  stream  caused  by 
the  formation  of  a  fluid  vein,  though  sonorous,  are  in  aU  probability 
largely  modified  by  the  conducting  properties  of  the  surrounding 
soUd  structures,  by  means  of  which  they  are  transmitted  to  the 
surface  of  the  chest,  and  hence  to  the  ear. 

The  presence  of  a  fibrous  cord  or  shred  of  membrane  capable  of 
free  vibrations  in  the  course  of  the  blood  stream  may  give  rise  to  a 
musical  murmur.  Such  conditions  may  exist  in  the  heart  when, 
in  consequence  of  the  improper  adaptation  of  the  margins  of  the 
valves  guarding  an  orifice,  the  free  edges  of  the  valvular  curtains  can 
vibrate,  or  when  a  shred  of  fibrin,  formed  as  the  result  of  some 
morbid  process,  hangs  loose  in  the  blood  stream. 

A  musical  murmur  can  also  be  produced,  under  certain  conditions, 
by  the  vibrations  of  a  fluid  vein  alone.  The  loudness  of  a  murmur 
depends  for  the  most  part  on  the  swiftness  of  the  flow  producing  it, 
and  this  is  determined  by  (a)  the  vis  a  tergo,  (b)  the  quality  of 
the  circulating  fluid,  and  {c)  the  degree  of  constriction  of  the  tube. 
If  the  velocity  of  the  flow  falls  below  a  certain  rate  no  murmur  is 
produced. 

A  murmur  is  propagated  in  the  direction  of  the  flow,  and  is  most 
distinctly  heard  immediately  to  the  distal  side  of  the  site  of  its 
production. 

This  statement  holds  good  with  respect  to  the  heart,  but  the  area 
of  audibihty  of  a  cardiac  murmur  is  greatly  modified  by  the  various 


METHODS   OF   DIAGNOSIS  55 

solid  structures  along  which  the  sonorous  vibrations  are  conducted 
to  the  surface  of  the  chest  wall. 

Cardiac  murmurs  are  distinguished  as  {a)  direct  or  obstructive,  or 
{b)  indirect  or  regurgitant,  according  as  they  are  produced  in  the 
course  of  or  against  the  natural  direction  of  the  blood  stream. 

Obstructive  murmurs  are  due  to — 

1.  The  narrowing  of  an  orifice,  the  result  of  a  local  constrictive 

process ;  or  an  impediment  to  the  onward  flow  of  blood 
through  an  opening  by  reason  of  an  outgrowth  or  projection 
from  its  valve,  or  from  adjacent  structures. 

2.  The  narrowing   of   an   orifice   relatively  to   the   size   of   the 

channel  situated  immediately  in  front  of  or  behind  it. 
In  such  cases  the  dimensions  of  the  orifice  remain  un- 
changed, while  the  cavity  or  lumen  of  the  structure  in 
immediate  relation  with  it,  either  anteriorly  or  posteriorly, 
becomes  dilated. 

Regurgitant  murmurs  are  due  to — 

1.  The  defective  closure  of  a  normally  closed  orifice,  the  result 

of  disease  affecting  the  valve  that  guards  it. 

2.  The  dilatation  of  an  orifice,  such  as  the  auriculo-ventricular, 

in  consequence  of  the  relaxation  and  stretching  of  its  mus- 
cular girdle,  so  that  the  curtains  of  its  valve  are  unable  to 
come  into  complete  apposition. 

3.  The  dilatation  of  an  orifice  owing  to  its  involvement  in  a  like 

process  affecting  primarily  the  channel  beyond  it,  with  the 
result  that  the  proper  adaptation  of  the  valvular  segments 
becomes  impossible. 

Murmurs  are  also  distinguished,  according  to  the  period  of  their 
occurrence  in  the  cardiac  cycle,  as  (a)  systolic  or  {b)  diastolic. 

A  murmur  that  is  heard  between  the  beginning  of  the  first  sound 
and  the  occurrence  of  the  second  is  called  "systolic,"  while  one 
which  appears  between  the-  beginning  of  the  second  sound  and  com- 
mencement of  the  first  is  called  "diastolic." 

Diastolic  murmurs  are  subdivided  into — 

1.  Murmurs  occupying  the  whole  diastole. 

2.  Murmurs  occupying  a  portion  only  of  the  diastole,  to  wit — ■ 

{a)  Early  diastolic  or  post  systolic 

{b)  Mid-diastolic 

{c]  Late  diastolic  or  presystolic 


56  DISEASES   OF   THE   HEART 

The  relation  of  murmurs  to  the  different  periods  of  the  cardiac 
cycle  may  be  diagrammatically  represented  as  follows  : — 

Systolic  Murmurs 


FIG.    9.       DIAGRAMMATIC    REPRESENTATION    OF   A   SYSTOLIC    MURMUR 

It  will  appear,  therefore,  that  systolic  murmurs,  due  to  organic 
disease,  and  produced  at  the  arterial  orifices  of  the  heart,  are 
indicative  of  obstruction  to  the  blood  stream,  whereas  at  the 
auriculo-ventricular  openings   they   are   significant   of  regurgitation. 

Conversely,  diastolic  murmurs  originating  at  the  arterial  orifices 
indicate  regurgitation,  and  at  the  auriculo-ventricular  openings, 
obstruction. 

Site  of  Production  and  Direction  of  Transmission  of  Organic 
Cardiac  Murmurs 

As  a  general  rule  a  murmur  is  most  distinctly  heard  over  that 
portion  of  the  chest  wall  which  is  nearest  to  the  site  of  its  pro- 
duction. The  relation  of  the  cardiac  orifices  to  the  thoracic  parietes 
has  already  been  defined  under  the  anatomical  description  of  the 
heart. 

The  deviations  from  the  general  rule  just  mentioned  are  numerous, 
and  depend,  for  the  most  part,  on  the  influence  exerted  by  the 
conducting  properties  of  {a)  the  solid  structures  interposed  between 
the  site  of  production  of  the  murmur  and  the  surface  of  the  chest, 
and  of  (b)  the  blood  current,  or,  as  it  usually  termed,  convection. 

The  modifications  in  the  area  of  audibility  of  a  murmur,  thus 
produced,  will  be  illustrated  in  the  following  account  of  the  subject. 

Mitral  Orifice. — Murmurs  which  are  due  to  lesions  at  the  left 
auriculo-ventricular   opening   may    be   either   systolic   or   diastolic, 


METHODS   OF  DIAGNOSIS 


57 


Diastolic  Murmurs 


FIG.   lO.     DIAGRAMMATIC   REPRESENTATION 
OF   AN    ENTIRE   DIASTOLIC    MURMUR 


FIG.   II.     DIAGRAMMATIC    REPRESENTATION 
OF  A   PRESYSTOLIC   MURMUR 


FIG-i   12      DIAGRAMMATIC   REPRESENTATION 
OF  AN   EARLY   DIASTOLIC   MURMUR 


FIG.    13.     DIAGRAMMATIC    REPRESENTATION 
OF   A   MID-DIASTOLIC   MURMUR 


58  DISEASES    OF   THE    HEART 

the  former  indicating  regurgitation  through,  the  latter  obstruction 
at  the  orifice. 

Systolic  7nitral  r?iurmurs. — These  are  most  distinctly  heard  in  the 
mitral  area,  inasmuch  as  they  are  conducted  thither  by  the  wall  of 
the  left  ventricle.  They  are  also  transmitted  (under  the  influence 
of  convection)  for  a  variable  distance  into  the  axilla,  and  may  be 
audible  as  far  outwards  as  the  angle  of  the  left  scapula.  Systolic 
mitral  murmurs  are  occasionally  heard  as  far  inwards  as  the  left 
sternal  edge,  in  the  tricuspid  area,  and  more  rarely  they  are 
conducted  upwards  as  high  as  the  third  or  second  rib.  In  ex- 
ceptional instances  systolic  mitral  murmurs  are  audible  in  the 
second  and  third  left  intercostal  spaces,  about  two  inches  from 
the  sternal  border,  and  in  this  situation  only. 

Diastolic  mitral  murmurs. — All  the  varieties  of  diastolic  murmur 
that  were  previously  enumerated  may  originate  at  the  mitral  orifice. 
Mitral  murmurs  which  occupy  the  whole  diastole  (or,  for  that  matter, 
any  part  of  it),  entire  diastolic  murmurs  as  they  have  been  called 
by  Dr.  Bristowe,  have  this  peculiarity  that  they  invariably  follow 
the  second  sound.  It  is  in  this  particular  that  they  differ  from 
aortic  diastolic  murmurs,  which,  whether  audible  in  the  mitral  area 
or  elsewhere,  accompany  and  partially  or  wholly  replace  the  second 
sound. 

Mitral  diastolic  murmurs  are  usually  most  distinctly  audible  in  the 
mitral  area,  and  for  the  reason  that  they  are  conducted  thither  by 
the  wall  of  the  left  ventricle. 

The  presystolic  murmur,  which,  for  the  sake  of  convenience  and 
on  account  of  its  importance,  will  be  considered  first,  is  best  heard 
immediately  above  and  to  the  inner  side  of  the  apex  beat,  and  its 
area  of  audibility  is  limited  to  this  situation  with  remarkable  con- 
stancy. It  is  occasionally  audible  as  far  to  the  right  as  the  left 
sternal  edge  and  upwards  as  high  as  the  third  rib.  Rarely,  too,  it  is 
conducted  into  the  axilla,  and  outwards  as  far  as  the  angle  of 
the  left  scapula. 

The  area  of  audibility  of  entire,  early,  and  mid-diastolic  murmurs 
corresponds,  in  the  main,  with  that  just  described,  though  it  is 
not  usually  so  localized. 

Combined  systolic  and  diastolic  mitral  murmurs. — Cases  of  pure 
mitral  obstruction  are  comparatively  rare,  since,  by  reason  of  the 
altered  condition  of  the  orifice  and  its  valve,  the  segments  of  the 
latter  are  seldom  able  to  come  into  effective  apposition,  and  con- 
sequently a  variable,  though  small,  amount  of  leakage  takes  place. 

The  systolic  murmur,  produced  by  this  means,  is  heard  in  the 
mitral  area,  but  it  is  seldom  well  conducted  into  the  axilla,  and 
is  rarely  if  ever  audible  at  the  angle  of  the  left  scapula. 

The  area  of  audibility  of  the  accompanying  presystolic  bruit  does 
not  dififer  from  that  previously  described  for  such  murmurs. 


METHODS    OF   DIAGNOSIS  59 

Aortic  Orifice.  —  Murmurs  originating  here  may  be  either 
systoHc  or  diastolic,  the  former  indicating  obstruction  at  the  orifice, 
dilatation  of  the  aorta,  or  roughening  of  its  hning  membrane  or 
of  the  cusps  of  the  valve,  the  latter,  regurgitation  through  the 
opening. 

Systolic  aortic  murmurs. — Systolic  murmurs  due  to  obstruction  at 
the  orifice  are  heard  best  in  the  aortic  area,  and  are  well  conducted 
upwards  (under  the  influence  of  convection)  into  the  neck,  especially 
on  the  right  side.  They  are  also  audible  over  the  upper  third  of 
the  sternum,  since  bone  is  a  good  conductor  of  sound. 

Murmurs  occasioned  by  atheromatous  disease  of  the  valve  or 
aorta  are  heard  in  the  same  situations,  but  they  tend  to  spread 
laterally  rather  than  upwards. 

Diastolic  aortic  murmurs. — The  area  over  which  these  murmurs 
may  be  heard  is  a  very  large  one.  A  diastolic  aortic  murmur  is 
most  distinctly  audible  at  one  time  in  the  aortic  area,  at  another 
in  the  mid-sternal  region  about  the  level  of  the  fourth  rib,  in  the 
mitral  area,  or  over  the  base  of  the  ensiform  cartilage.  It  is  usually 
well  conducted  downwards  along  the  right  and  left  edges  of  the 
sternum,  and  along  an  oblique  line  leading  from  the  second  right 
costal  cartilage,  at  its  junction  with  the  sternum,  to  the  apex  beat. 

A  diastolic  aortic  murmur  is  sometimes  audible  at  the  apex  only, 
and  in  such  cases  may  closely  resemble  the  presystolic  murmur  that 
is  associated  with  mitral  stenosis.  The  reason  for  this  will  be  con- 
sidered under  the  heading  of  the  valvular  lesion  in  question. 

An  aortic  diastolic  murmur  may  also  be  heard  in  the  neck  over 
the  carotid  arteries,  and  most  distinctly  on  the  right  side. 

Combined  systolic  and  diastolic  aortic  murmurs. — The  two  mur- 
murs are  observed  over  their  respective  areas  of  audibility,  as  above 
described.  In  those  situations  where  the  areas  of  audibility  overlap 
a  "  to  and  fro  "  murmur  is  heard. 

Pulmonary  Orifice. — Murmurs  due  to  structural  disease  at  this 
orifice,  apart  from  congenital  conditions,  are  rare.  Nevertheless 
systoHc  and  diastoHc  murmurs,  indicating  stenosis  of  the  opening 
and  incompetence  of  the  valve  respectively,  are  occasionally 
observed. 

Systolic  pulmonary  murmurs. — These  are  heard  most  distinctly  in 
the  second  left  interspace  close  to  the  sternum,  and  are  transmitted 
upwards  and  to  the  left  for  a  short  distance.  They  may  also  extend 
to  the  right  as  far  as  the  aortic  area  on  a  level  with  the  second  inter- 
space.    They  are  inaudible  in  the  neck. 

Diastolic  pulmonary  murmurs. — These  are,  as  a  rule,  most  plainly 
audible  in  the  pulmonic  area,  and  are  conducted  downwards  along 
the  left  sternal  edge  as  far  as  the  base  of  the  ensiform  cartilage. 
They  may  be  heard  over  any  portion  of  the  right  ventricle. 


6o  DISEASES   OF   THE   HEART 

Tricuspid  Orifice. — Murmurs  produced  at  this  orifice  may  be 
either  systolic  or  diastolic,  and  have,  mutatis  miita?idis,  the  same 
significance  as  those  heard  at  the  mitral  opening. 

Systolic  tricuspid  murmurs. — These  are  heard  most  distinctly  in  the 
tricuspid  area,  and  are  conducted  by  the  right  ventricle  to  the  right, 
and  upwards  along  the  sternal  edge  as  high  as  the  fourth  interspace. 

Diastolic  tricjispid  murmurs. — A  presystolic  murmur,  indicating 
tricuspid  stenosis,  is  sometimes  heard  at  the  left  sternal  edge,  about 
the  level  of  the  fourth  and  fifth  costal  cartilages,  and  over  the  base 
of  the  ensiform  cartilage. 

Combined  systolic  and  diastolic  tricuspid  murmurs. — A  systolic  and 
presystolic  murmur  are  occasionally  heard  together  in  the  tricuspid 
area. 

Associated  murmurs. — It  not  infrequently  happens  that  more  than 
one  orifice  of  the  heart  is  the  seat  of  disease  at  the  same  time,  and 
in  such  an  event  murmurs  with  different  sites  of  production  may 
coexist. 

The  most  common  association  is  that  of  systolic  and  diastolic 
aortic  murmurs,  with  a  systolic  mitral  bruit,  and  then  either  of  the 
former  with  the  latter.  Combined  systolic  and  diastoHc  murmurs 
produced  at  the  aortic  and  mitral  openings  may  also  coexist,  and 
more  rarely  still  combined  or  single  aortic  murmurs  may  be 
associated  with  a  presystolic  mitral  bruit.  A  systolic  or  presystolic 
mitral  murmur,  or  a  combination  of  the  two,  is  not  uncommonly 
associated  with  a  systolic  murmur  of  tricuspid  origin. 

Apart  from  congenital  conditions,  a  presystolic  tricuspid  murmur 
is  almost  invariably  associated  with  a  mitral  presystolic  bruit. 

With  respect  to  the  association  of  murmurs  which  are  produced 
on  the  left  and  right  sides  of  the  heart,  it  should  be  noted  that  the 
relation  of  the  lesions  giving  rise  to  them  is  nearly  always  one  of 
cause  and  effect. 

The  Character  of  Organic  Murmurs 

Cardiac  murmurs  are  described  as  blowing,  rasping,  purring, 
rumbling,  etc.,  according  to  the  fancy  of  the  observer. 

These  terms  apply,  of  course,  to  the  quality  of  the  sound,  which 
is  of  little  clinical  importance. 

Systolic  mitral  murmurs  are  usually  soft  and  blowing,  and  some- 
times possess  a  musical  character,  whereas  systolic  aortic  murmurs 
are  commonly  rough  and  rasping. 

The  presystolic  bruit  due  to  mitral  obstruction  is  peculiarly  and 
characteristically  rough  and  rumbling,  and  increases  in  intensity  up 
to  the  first  sound,  at  which  it  abruptly  terminates.  Presystolic 
tricuspid  murmurs  exhibit  similar  qualities. 

Diastolic  murmurs  produced  at  the  aortic  orifice  are  usually  soft 
and  blowing,  and  they  gradually  diminish  in  intensity  from  their 
commencement  with  the  second  sound  to  their  termination.    They  do 


METHODS  OF  DIAGNOSIS  6i 

not,  however,  always  possess  these  characters,  for,  as  has  already 
been  pointed  out,  a  murmur  due  to  aortic  regurgitation  is  sometimes 
audible  at  the  apex  only,  and  may  then  be  indistinguishable,  so  far  as 
its  character  is  concerned,  from  that  associated  with  mitral  obstruction. 
The  distinctness  with  which  a  cardiac  murmur  is  heard  depends 
for  the  most  part  on  posture,  on  the  quantity  and  conducting  quality 
of  the  material  interposed  between  the  site  of  production  of  the 
murmur  and  the  ear,  and  on  the  loudness  of  the  murmur. 

Unless  considered  in  the  light  of  previous  observations,  the  loud- 
ness of  a  murmur  is  of  Uttle  or  no  diagnostic  or  prognostic  value. 
It  depends  mainly  on  the  swiftness  of  the  blood  current,  and  in  the 
case  of  the  heart  this  will  be  determined  by  the  force  of  the  auri- 
cular or  ventricular  contraction,  as  the  case  may  be,  and  by  the 
condition  of  arterial  tension. 

Speaking  generally,  a  loud  murmur  is  of  less  import  than  a  soft 
one,  as  it  is  an  indication  that  the  heart  is  acting  forcibly. 

Gradual  increase  in  the  intensity  of  a  murmur  is  a  good  prog- 
nostic sign,  in  so  far  as  it  is  indicative  of  improving  cardiac  vigour. 
On  the  other  hand,  sudden  or  gradual  decrease  in  the  intensity  of  a 
murmur  is  often  significant  of  serious  failure  of  the  power  of  the 
heart. 

A  soft  murmur  is,  however,  compatible  with  very  slight  damage 
either  to  the  myocardium  or  endocardium. 

The  subject  will  be  again  referred  to  under  the  general  account  of 
the  prognosis  in  valvular  affections  of  the  heart. 

The  Rhythm  of  Organic  Cardiac  Murmurs 

It  has  already  been  pointed  out  that,  with  regard  to  their  position 
in  the  cardiac  cycle,  murmurs  may  be  either  systolic  or  diastolic. 
Their  time  relations  should  be  gauged  clinically  by  reference  to  the 
sounds  of  the  heart,  to  the  impulse  of  the  organ,  and  to  the  carotid 
pulse,  which  for  all  practical  purposes  is  synchronous  with  the 
ventricular  systole. 

It  must  be  borne  in  mind  that  palpation  of  the  apex  beat  does 
not  always  afford  reliable  information  as  to  the  time  of  the  con- 
traction of  the  ventricles,  as  may  be  demonstrated  in  some  cases 
of  aortic  regurgitation. 

With  reference  to  the  position  of  murmurs  in  the  cardiac  cycle, 
two  additional  points  remain  to  be  mentioned,  viz.  (i)  the  relation 
of  the  murmur  to  the  sound  of  the  heart  with  which  it  is  associated, 
and  (2)  the  duration  of  the  murmur. 

Thus,  by  way  of  illustrating  the  first  point,  a  systolic  murmur 
produced  at  the  mitral  orifice  may  wholly  or  partially  replace  the 
first  sound  of  the  heart. 

If  the  murmur  wholly  obscures  the  first  sound,  the  indication  is 
that  there  is  an  excessive  production  of  sonorous  vibrations  at  the 
orifice,  or  that  the  valvular  segments  are  unable  to  undergo  sufficient 
tension  to  produce  a  sound.     Under  either  supposition  the  inference 


62  DISEASES    OF   THE  .HEART 

is  that  the  amount  of  regurgitation  must  be  considerable.  If,  on 
the  other  hand,  the  murmur  follows  and  only  partially  obscures  the 
sound,  it  is  obvious  that  the  segments  of  the  auriculo-ventricular 
valve  are  able  to  come  together,  but  are  unable  to  remain  in  apposi- 
tion, which  argues  but  a  slight  amount  of  leakage  through  the 
opening. 

Again,  a  diastolic  murmur  produced  at  the  aortic  orifice  may 
wholly  or  partially  replace  the  second  sound.  If  the  second  sound 
is  inaudible  it  means  that  the  valvular  cusps  fail  to  offer  any 
effective  check  to  the  backflow  of  blood,  and  therefore  that  there 
must  be  a  large  amount  of  regurgitation.  If,  on  the  other  hand, 
the  murmur  follows  the  second  sound,  or  only  slightly  obscures 
it,  the  valve  must  still  offer  a  hindrance  to  the  regurgitant 
current,  and  consequently  the  leakage  through  the  opening  can  be 
but  slight. 

These  considerations,  while  affording  a  valuable  means  of  esti- 
mating the  degree  of  incompetence  of  a  valve,  are  not  absolute, 
and  they  must  be  weighed  in  conjunction  with  the  other  indications 
of  the  extent  of  the  valvular  insufficiency. 

The  duration  of  a  murmur  is  of  little  clinical  significance. 

A  long  murmur,  which  depends  on  valvular  incompetence,  fre- 
quently indicates  slight  disease  and  a  forcible  action  of  the  heart. 
On  the  other  hand,  a  short  murmur  is  sometimes  a  sign  of  serious 
failure  of  the  cardiac  power. 

2.  Hsemic  murmurs. — The  method  of  production  of  hgemic 
or  functional  murmurs  (as  they  are  sometimes  termed)  has  long 
been  a  subject  of  controversy,  and  still  remains  undetermined. 
There  can  be  little  doubt,  however,  that  the  production  of  a 
haemic  murmur  depends,  as  in  the  case  of  an  organic  murmur, 
on  the  formation  of  a  fluid  vein,  which  is  sonorous.  If  the 
conditions  under  which  a  fluid  vein  may  be  formed  can  be  shown 
to  be  present  in  anaemia,  there  is  no  necessity  to  endeavour  to 
explain  the  occurrence  of  hjemic  murmurs  on  other  grounds.  An 
attempt  will  be  made  to  show  that  such  conditions  may  exist,  but 
it  wall  also  be  necessary  to  briefly  review  the  other  chief  theories 
which  have  been  advanced  to  explain  the  formation  of  these 
murmurs. 

The  order  in  which  hsemic  murmurs  appear  in  anaemia  is  usually 
as  follows  : — 

1.  The  venous  hum  or  "bruit  de  diable"  in  the  neck, 

2.  A  systolic  murmur  in  the  pulmonic  area. 

3.  A  systolic  murmur  in  the  mitral  area. 

4.  A  systolic  murmur  in  the  tricuspid  area. 

5.  A  systolic  murmur  in  the  aortic  area. 


METHODS   OF   DIAGNOSIS  63 

Site  of  Production  and  Direction  of  Transmission  of  Cardiac  Murmurs 
due  to  Anaemia 
The  venous  hum  which  may  be   heard  in  the  neck  in  cases  of 
anaemia,  will  be  considered  under  its  appropriate  heading. 

Cardiac  murmurs  of  hsemic  origin  will  be  taken  in  the  order  of 
their  usual  appearance. 

Pulmonic  orifice. — A  systolic  bruit,  which  is  most  distinctly  audible 
in  the  second  left  intercostal  space  close  to  the  sternum,  or,  in  other 
words,  in  the  pulmonic  area,  is  the  earliest  and  most  constant  of 
the  cardiac  murmurs  that  are  found  in  association  with  ansemia. 

The  area  of  audibility  of  the  murmur  as  given  here  is  not 
admitted  by  all  writers  on  the  subject,  nevertheless  the  majority 
are  agreed  that  the  bruit  appears  soonest,  and  is  heard  best,  in  this 
situation.  It  is  in  all  probability  produced  at  the  pulmonic  orifice, 
and  for  the  following  reasons. 

In  anemia,  from  whatever  cause,  there  is  present  a  general 
muscular  malnutrition,  and  the  heart  suffers  in  common  with  the 
rest  of  the  contractile  tissues.  Owing  to  the  comparative  thinness 
of  its  walls,  the  right  ventricle  feels  the  effect  of  this  nutritional 
impairment  at  an  early  period  of  the  disease,  and  a  variable  degree 
of  dilatation  of  the  ventricular  cavity  ensues.  Consequently  the 
orifice  of  the  pulmonic  artery,  which  by  reason  of  its  dense 
fibrous  girdle  remains  unaltered  in  size,  becomes  relatively  con- 
stricted as  regards  the  cavity  of  the  ventricle,  and  hence  the 
conditions  for  the  production  of  a  fluid  vein  are  present.  This 
view,  too,  would  explain  the  presence  of  a  murmur,  even  if,  as 
Duroziez  asserts,  the  heart  and  its  cavities  are  diminished  in  size  in 
anemia,  for  then  the  pulmonic  orifice  would  be  relatively  dilated. 
It  is  possible,  indeed  probable,  that  the  alteration  in  the  quality  of 
the  circulating  fluid  may  also  be  a  factor  in  the  production  of  the  fluid 
vein.  A  fall  of  blood  pressure  in  the  aorta  or  pulmonary  artery  as 
the  case  may  be  is  also  a  contributory  factor  in  the  production  of  a 
functional  systolic  murmur  at  the  orifices  of  these  vessels. 

Balfour  considers  that  the  murmur  under  consideration  is  due 
to  mitral  regurgitation,  which  causes  a  vibration  of  the  walls  of  the 
left  auricular  appendix,  and  therefore  that  the  murmur  is  heard 
most  distinctly  over  the  position  of  the  appendix,  i.e.  in  the  second  left 
intercostal  space  one  and  a  half  to  two  inches  outside  the  left  sternal 
edge.  Apart  from  the  fact  that  the  area  in  which  the  murmur 
is  most  plainly  audible  is  not  located  by  the  majority  of  observers 
in  the  situation  described  by  Balfour,  it  has  been  shown  that  in 
a  large  number  of  cases  of  ansemia  the  left  auricular  appendix 
does  not  come  into  contact  with  the  chest  wall. 

Moreover,  it  is  difficult  to  suppose  that  the  small  amount  of 
regurgitation  which  takes  place  could  cause  any  audible  vibration 
of  the  auricular  walls,  seeing  that  in  structural  disease  of  the 
mitral  valve,  with  considerable  leakage,  systolic  murmurs  are  rarely 
heard  in  the  situation  described  by  Balfour. 


64  DISEASES    OF   THE    HEART 

Russell's  theory,  which  accounts  for  the  murmur  by  the  pressure 
of  a  dilated  auricle  on  the  pulmonary  artery  causing  a  local  narrow- 
ing of  the  vessel  and  hence  a  fluid  vein,  is  equally  improbable. 
There  is  no  proof  that  the  auricle  is  distended  in  anaemia,  and 
furthermore,  there  is  direct  evidence  that  when  the  auricle  is 
dilated,  as  in  mitral  stenosis,  no  pressure  is  exerted  on  the 
pulmonary  artery,  or  at  all  events  not  sufficient  to  produce  a 
murmur. 

Chauveau  supposes  that  in  anaemia  the  total  quantity  of  blood 
in  the  body  is  diminished,  and  this  results  in  a  partial  collapse 
of  the  capillaries,  small  and  medium-sized  arteries  and  veins,  and 
of  the  heart  and  its  orifices.  The  aorta  and  pulmonic  artery, 
owing  to  the  anatomical  structure  of  their  walls,  are  unable  to 
accommodate  themselves  to  the  altered  circulatory  conditions, 
and  consequently  they  become  relatively  dilated  as  regards  their 
respective  orifices,  and  thus  the  conditions  for  the  production  of 
a  fluid  vein  are  produced. 

It  has  not  been  proved  that  the  total  quantity  of  blood  is 
diminished  in  anaemia ;  moreover,  partial  collapse  of  the  orifices 
of  the  aorta  and  pulmonic  artery  would  seem  as  difficult  of 
accomplishment  as  of  the  vessels  themselves. 

According  to  Hayden,  two  factors  enter  into  the  causation  of 
haemic  murmurs,  viz.  (i)  friction  of  the  blood  corpuscles  against 
one  another  and  against  the  edges  of  the  cardiac  orifices  and  walls 
of  the  vessels,  and  (2)  vibrations  of  the  heart  and  walls  of  the 
vessels. 

It  is  by  no  means  certain  that  increased  friction  between  the 
blood  corpuscles,  etc.,  could  give  rise  to  sonorous  vibrations. 
Moreover,  if  this  were  possible,  the  occurrence  and  intensity  of 
the  bruit  thereby  produced  should  be  regulated  by  the  degree 
of  anaemia,  which  is  not  the  case  with  respect  to  haemic 
murmurs. 

Explanations  of  the  mode  of  formation  of  haemic  murmurs 
based  on  neuro-muscular  causes,  such  as  those  advanced  by  Dr. 
Sansom,  can  hardly  be  considered  satisfactory  in  the  present  state 
of  our  knowledge  of  these  conditions. 

Foxwell  (Bradshaw  Lecture,  1899)  contends  that  the  systolic 
murmur  heard  in  the  second  and  third  intercostal  spaces  in  cases 
of  cardiac  debility  (due  to  anaemia  and  other  causes)  depends  on 
a  localized  dilatation  of.  the  conus  arteriosus  and  pulmonary  artery. 
He  states  that  dilatation  of  the  conus  arteriosus  and  pulmonary 
artery  is  constantly  found  post  mortem  in  patients  who  during  life 
exhibited  this  functional  pulmonary  murmur,  and  he  advances  the 
following  arguments  with  the  object  of  showing  that  this  association 
is  one  of  cause  and  effect :  — 

I.  The  pulmonary  orifice  is  not  increased  in  size,  and  therefore 
becomes  relatively  constricted  as  regards  the  enlarged  conus, 


METHODS   OF   DIAGNOSIS  65 

with  the  consequent  production  of  the  necessary  conditions 
lor  the  formation  of  a  fluid  vein  and  hence  of  a  murmur. 

2.  The  dilatation  of  the  conus  carries  the  orifice  of  the  pulmonary 

artery  upwards,  so  that  the  valve  comes  to  lie  vertically  over 
the  bifurcation  of  the  vessel,  which  is  a  fixed  point.  The 
shortening  of  the  artery,  produced  by  this  means,  renders  its 
walls  less  taut,  and  thereby  conduces  to  a  bagging  of  the 
vessel  with  each  systolic  incursion  of  blood.  This  condition 
would  result  in  the  formation  of  eddies,  and  hence  of  a 
murmur. 

3.  The  want  of  space  necessary  to  accommodate  the  increased 

size  of  the  pulmonary  artery  would  lead  to  the  compression 
of  the  lax  arterial  wall  by  the  comparatively  rigid  parietes  of 
the  chest  and  also  by  the  aortic  arch,  and  this,  acting  as  a 
partial  constriction,  would  tend  to  the  production  of  eddies 
and  a  murmur. 

4.  Owing  to  the  greater  extensibility  of  the  anterior  surface  of 

the  conus  and  the  comparatively  firm  attachment  of  the 
posterior  wall  of  the  pulmonary  artery  to  the  aorta,  the 
anterior  wall  of  the  pulmonary  artery  is  carried  up  further 
than  the  posterior  wall.  As  a  consequence  of  this  the 
plane  of  the  valve  ring  is  not  perpendicular  to  the  longi- 
tudinal axis  of  the  artery,  and  the  systolic  incursion  of 
blood  would  therefore  tend  to  be  directed  against  the 
wall  of  the  vessel,  and  in  this  way  eddies  might  be  formed 
and  consequently  a  murmur. 

Dr.  Foxwell  also  brings  forward  direct  experimental  evidence  in 
support  of  his  contention.  Indeed,  in  the  face  of  the  arguments 
and  experiments  advanced  by  him,  it  is  difficult  if  not  impossible 
to  resist  the  conclusion  that  the  pulmonary  systolic  murmur  heard 
in  cases  of  cardiac  debility  is  due  to  the  dilatation  of  the  conus 
arteriosus  and  pulmonary  artery. 

Mitral  orifice. — The  systolic  murmur,  which  is  audible  at  the 
apex  of  the  heart  in  some  cases  of  ansemia,  is  due  to  regurgitation 
through  the  mitral  opening.  It  is  heard  most  plainly  in  the  mitral 
area,  and  is  conducted  with  a  variable  degree  of  distinctness  into 
the  axilla,  and  is  occasionally  audible  at  the  angle  of  the  left 
scapula. 

Regurgitation  through  the  mitral  orifice  consequent  on  anaemia 
may  be  the  result  of — 

I.  Enfeeblement  of  the  muscular  fibres  surrounding  the  opening, 
whereby  the  orifice  is  not  sufficiently  constricted  to  permit 
the  proper  adaptation  of  the  valvular  curtains. 

z.  Dilatation  of  the  left  ventricle  from  failure  of  its  muscular 
walls,  which  may  be  due  to  malnutrition  of  the  myocardium, 
F 


66  DISEASES    OF   THE    HEART 

or  to  the  high  arterial  tension  that  is  sometimes  associated 
with  anaemia. 

3.  Enfeeblement  of  the  rausculi  papillares  from  similar  causes. 

Under  normal  conditions  the  closure,  or  in  other  words  the 
proper  adaptation  of  the  curtains  of  the  auriculo-ventricular  valves, 
{i.e.  mitral  and  tricuspid)  is  effected,  during  systole,  by  means  of  (a) 
the  constriction  of  the  orifices  by  the  contraction  of  their  respective 
muscular  sphincters  and  {^)  the  maintenance  of  the  levels  of  the 
valvular  segments,  and  thus  the  prevention  of  their  retroversion 
into  the  auricles  by  the  shortening  of  the  musculi  papillares. 

Failure  in  the  proper  performance  of  either  of  these  functions  may 
prevent  the  perfect  apposition  of  the  valvular  flaps,  and  thus  render 
the  valve  incompetent. 

Dilatation  of  the  ventricles  acts  by  increasing  the  size  of  the 
auriculo-ventricular  openings,  so  that  the  contraction  of  the  muscular 
sphincters  cannot  reduce  their  dimensions  sufficiently  to  enable  the 
curtains  of  the  valves  to  come  into  complete  apposition,  and  hence 
leakage  takes  place  into  the  auricles. 

Tricuspid  orifice. — A  systolic  murmur,  indicative  of  tricuspid 
regurgitation  and  audible  in  the  tricuspid  area,  is  sometimes  ob- 
served with  anaemia.  The  mechanism  of  its  production  has  already 
been  explained. 

It  is  certainly  not  a  little  remarkable  that,  so  far  as  the  auscultatory 
evidence  is  concerned,  mitral  regurgitation  always  precedes  leakage 
through  the  tricuspid  valve  in  anaemia,  since  a  pj'iori  it  would 
seem  likely  that  the  right  ventricle,  and  with  it  the  tricuspid  opening, 
should  undergo  dilatation  before  the  left.  At  the  same  time,  in- 
competence of  the  tricuspid  valve,  more  especially  when  this  is 
slight,  may  exist  without  giving  rise  to  any  auscultatory  signs,  and 
it  may  be  that  herein  lies  the  explanation  of  the  late  appearance 
of  the  murmur. 

Aortic  orifice. — The  systolic  murmur,  which  may  be  audible  in  the 
aortic  area  in  cases  of  anaemia,  is  in  all  probability  due  to  relative 
stenosis  of  the  aortic  orifice,  by  reason  of  the  dilatation  of  the  left 
ventricle  while  the  size  of  the  opening  remains  unchanged. 

Speaking  generally,  the  area  of  audibility  of  hasmic  murmurs 
formed  at  any  of  the  cardiac  orifices  corresponds  with  that  of  organic 
murmurs,  of  like  rhythm,  produced  in  the  same  situations,  though 
the  former  are  seldom  so  widely  or  so  clearly  conducted  as  the  latter. 

Character  of  Haemic  Murmurs 

Heemic  murmurs  have  usually  a  soft  and  blowing  character, 
though  those  produced  at  the  pulmonic  orifice  are  sometimes 
remarkably  rough  and  loud. 


METHODS   OF   DIAGNOSIS  ^7 


Rhythm  of  Haemic  Murmurs 

Cardiac  murmurs  due  to  anaemia  are  invariably  systolic  as  regards 
their  time  relation  to  the  cycle  of  the  heart. 


{b)  Exocardial  Adventitious  Sounds 

I.  Friction  sounds.  Pericardial. — In  health  the  movements  of 
the  parietal  and  visceral  layers  of  the  pericardium  on  each  other  give 
rise  to  no  appreciable  sound.  When  these  normally  smooth  surfaces 
become  roughened  by  disease,  friction  sounds  coincident  with  the 
movements  of  the  heart  may  be  produced.  Friction  sound  may  be 
audible  over  any  portion  of  the  prsecordial  area,  but  as  a  rule  it 
appears  earliest  and  is  most  distinct  over  the  right  ventricle  and  base 
of  the  heart.  Unless  it  is  very  loud,  friction  sound  can  be  heard 
over  the  site  of  production  only,  and  consequently  its  area  of  audi- 
bihty  is  usually  limited  by  the  praecordial  outline ;  a  point  of  some 
value  in  the  differential  diagnosis  of  pericardial  from  endocardial 
sounds,  since  the  latter  are  audible  outside  this  area. 

A  peculiar  form  of  friction  sound  is  sometimes  heard  over  the 
right  ventricle  at  the  level  of  the  fifth  and  sixth  intercostal  spaces 
close  to  the  left  sternal  edge  and  over  the  base  of  the  ensiform  car- 
tilage. It  is  possibly  associated  with  the  formation  of  the  "white 
patch"  which  may  be  observed  on  the  underlying  portion  of  the 
pericardium  covering  the  heart.  The  sound  is  systolic  as  regards  its 
relation  to  the  cardiac  cycle,  and  may,  at  one  time,  roughly  resemble 
a  reduplication  of  the  first  sound,  at  another,  an  endocardial  bruit. 
It  may  vary  in  character  between  a  faint  click  and  a  definite  rub,  and 
as  a  rule  the  intensity  of  the  sound  is  greatly  modified  by  changes  in 
the  position  of  the  body.  The  sound  is  most  commonly  observed 
in  downward  displacement  of  the  heart  due  to  emphysema,  but  it 
may  be  present  under  apparently  normal  conditions. 

Pericardial  friction  sound  is  described  as  scraping,  rubbing,  creaking, 
grating,  rasping,  etc.,  and  it  conveys  to  the  observer  the  impression  that 
it  is  produced  close  to  the  ear.  The  intensity  of  the  sound  is  compara- 
tively uniform  from  beginning  to  end,  thus  differing  from  endocardial 
murmurs  which  usually  have  a  crescendo  or  diminuendo  character. 
Moreover,  the  loudness  of  a  pericardial  friction  sound  is  commonly 
markedly  modified  by  (a)  pressure  with  the  stethoscope,  {b)  deep 
inspiration  or  expiration,  and  ic)  changes  in  position  of  the  body. 
Furthermore,  friction  sound  may  change  its  site  of  maximum  intensity 
from  day  to  day — indeed  it  may  do  so  while  under  observation — 
though,  unlike  reduplication  of  the  heart  sounds,  it  does  not  show- 
intermissions. 

Friction  sound,  as  has  already  been  stated,  corresponds,  not 
with  the  sounds  of  the  heart,  but  with  the  movements  of  the 
organ.      Consequently  it  usually  has  a  "to  and  fro"  rhythm,   i.e. 


68  DISEASES   OF  THE   HEART 

systolic  and  diastolic,  corresponding  with  the  contraction  and  relaxa- 
tion of  the  ventricles.  It  may,  however,  exhibit  a  triple  rhythm, 
owing  to  the  systole  of  the  auricles,  and  the  sound  thus  produced  is 
presystolic  in  its  relation  to  the  cardiac  cycle.  The  presystolic 
friction  sound  is  heard  most  distinctly  in  the  second  and  third  left 
intercostal  spaces  about  one  and  a  half  to  two  inches  from  the  sternal 
border.  The  relation  of  the  friction  sound  to  the  cardiac  cycle  may 
vary  from  day  to  day.  At  one  time  it  may  be  systolic  and  diastolic, 
at  another  presystolic,  systolic,  and  diastolic,  or  again  i,t  may  be 
systolic  or  diastolic  only.  A  sound  which  is  observed  to  vary  thus 
in  its  relation  to  the  cardiac  cycle  is  almost  certainly  pericardial  in 
point  of  the  site  of  its  production. 

It  sometimes  happens  that  both  air  and  fluid  are  present  at  the 
same  time  in  the  pericardial  sac.  Under  such  conditions  sounds 
corresponding  with  the  movements  of  the  heart,  and  having  various 
characters,  may  be  heard.  Thus  splashing  or  gurgling  sounds  are 
sometimes  observed,  and  these  have  been  compared  to  the  noise 
produced  by  a  water-wheel  in  motion,  and  hence  have  been  called 
"  water-wheel  sounds."  On  other  occasions  an  amphoric  echo  of 
the  heart  sounds  or  of  pericardial  friction  sound  is  produced.  These 
signs  do  not  persist  many  days,  and  are  invariably  of  the  gravest 
import. 

Pleural. — A  pleural  friction  sound  has  occasionally  a  "to  and 
fro  "  character  communicated  to  it  by  the  movements  of  the  heart. 
In  such  cases  the  sound,  as  a  rule,  ceases  when  a  deep  inspiration 
is  made  and  the  breath  is  held. 

Pleuro-perkai'dial. — Inflammation  of  the  pleura  over  the  heart 
may  lead  to  the  production  of  sounds  very  like  those  caused  by 
pericardial  friction.  The  differential  diagnosis  between  the  two 
may  be  difficult,  but  in  the  case  of  pleuro-pericardial  friction  sound, 
the  site  over  which  it  is  most  distinctly  heard  is  usually  along  the 
border  of  the  left  ventricle,  and  not  over  the  base  of  the  heart, 
or  right  ventricle,  and  further  it  is,  as  a  rule,  markedly  modified 
by  the  respiratory  movements.  Thus  pleuro-pericardial  friction 
sound  often  disappears  at  the  end  of  expiration,  or  when  the  breath 
is  held ;  whereas  during  inspiration,  when  the  pleural  surface  is  more 
closely  applied  to  the  pericardium,  it  is  increased  in  intensity. 
Pericardial  friction  sound,  on  the  other  hand,  is  not  annulled  by 
holding  the  breath,  and  is  loudest  during  expiration. 

2.  Murmurs.  Cardio-pulmonary. — It  will  be  most  convenient 
to  consider  these  under  sounds  of  exocardial  origin,  though,  as 
will  be  seen,  they  are  endocardial  as  regards  site  of  production 
in  many  cases.  They  have  one  feature  in  common,  which  is 
that  they  all  depend  in  the  first  instance  on  changes  outside  the 
heart. 


METHODS  OF   DIAGNOSIS  69 

Cardio-pulmonary  murmurs  are  produced  in  a  variety  of  ways, 
which  may  be  arranged  as  follows  : — 

1.  Displacements  of  the  heart  due  to  disease  of — 

(a)  The  thorax 
(^)  The  pleurae 

(c)  The  lungs 

(d)  The  abdomen 

2.  Pressure  on  the  heart  due  to  disease  of  the  left  pleura. 

3.  Changes  in  the  lung  overlying  the  heart. 

I.  Displacements  of  the  Heart  due  to  Disease  of 

(a)  The  thorax. — In  severe  cases  of  deformity  of  the  thorax  the 
heart  is  always  more  or  less  displaced,  and  a  systolic  murmur  may 
be  heard  over  some  portion  of  the  altered  prascordial  area,  and 
is  produced  most  probably  by  the  dislocation  and  consequent 
twisting  of  the  great  vessels  at  the  base  of  the  heart. 

{b)  The  pleurcB. — A  systoUc  bruit  is  occasionally  heard  in  the 
pulmonic  or  aortic  area  in  cases  of  extensive  pleural  effusion  on 
either  side.  It  is  in  all  probability  produced  in  the  pulmonary 
artery  or  aorta,  as  the  case  may  be,  in  consequence  of  the  slight 
twisting  of  these  vessels,  which  may  accompany  considerable  dis- 
placement of  the  heart.  The  murmur  disappears  when  the  fluid 
has  been  removed  and  the  heart  has  returned  to  its  normal 
situation. 

{c)  The  lungs.  —  Displacement  of  the  heart  following  pleuro- 
pericardial  adhesions  and  the  contraction  of  a  cavity,  or  cirrhosis 
of  either  lung,  may  give  rise  to  a  systolic  bruit,  which  is  usually 
most  distinctly  heard  in  the  second  interspace  to  the  right  or  left  of 
the  sternum,  according  as  the  right  or  left  lung  is  affected.  The 
murmur  is  also  often  distinctly  audible  over  the  pulmonary  cavity 
and  sometimes  over  the  whole  of  the  affected  side.  It  is  as  a  rule 
most  intense  during  inspiration.  The  mechanism  of  its  production 
is  in  all  probability  similar  to  that  suggested  in  the  preceding 
paragraph. 

{d)  The  abdomen. — A  systolic  murmur  audible  at  the  base  or 
apex  of  the  heart  may  be  due  to  the  displacement  of  the  organ  by 
a  large  fluid  or  gaseous  effusion  into  the  peritoneal  cavity.  Re- 
moval of  the  effusion  is  followed  by  disappearance  of  the  bruit. 

2.  Pressure  on  the  Heart  due  to  Disease  of  the  Left  Pleura 

A  systolic  murmur  audible  over  the  heart  and  left  side  of  the 
chest  sometimes  follows  inflammation  of  the  left  pleura.  In  cases 
of  this  kind  the  lung  becomes  fixed  over  the  pericardium  by  pleural 
adhesions,  and  the  heart  is  more  or  less  pressed  upon  by  the 
thickened  pleura.      The   murmur  is   supposed  to  be  due  to  the 


70  DISEASES   OF  THE   HEART 

sudden  displacement  of  air  in  the  larger  bronchi,  as  the  result  of 
the  impact  of  ihe  contracting  ventricle  on  the  surrounding  lung 
tissue,  which  has  undergone  partial  consolidation.  The  bruit  is 
usually  systolic  in  its  relation  to  the  cardiac  cycle,  but  it  may  be 
diastolic,  and  it  is  heard  most  distinctly  during  inspiration.  It 
usually  disappears  when  the  breath  is  held. 

3.  Changes  in  the  Lung  Overlying  the  Heart 

Pulsating  crepitations  or  rales  are  sometimes  heard  at  the  apex  of 
the  heart  in  morbid  conditions  of  the  lung  overlying  the  organ. 
They  disappear  when  the  breath  is  held  after  a  deep  expiration. 

A  systolic  murmur  audible  at  the  apex  may  be  observed  when 
the  overlapping  lung  is  partially  consolidated,  and  its  mode  of 
production  has  already  been  explained. 

A  systolic  murmur  audible  in  the  pulmonic  area  is  of  fairly 
common  occurrence  in  tubercular  disease  of  the  upper  lobe  of  the 
left  lung.  The  pulmonary  artery  is  in  all  probability  displaced  or 
pressed  upon  by  enlarged  glands,  or  consolidated  lung,  and  the 
local  narrowing  of  the  vessel  thus  produced  results  in  the  formation 
of  a  fluid  vein,  and  hence  the  murmur. 


The  Differential  Diagnosis  of  Endocardial  and 
Exocardial  Murmurs 

The  size  of  the  various  chambers  composing  the  heart  should 
first  be  ascertained  in  the  manner  described  under  "  Physical 
Diagnosis,"  and  any  changes  that  obtain  should  be  weighed  in 
conjunction  with  the  known  effects  of  any  particular  valvular  lesion 
or  other  morbid  cardiac  condition  which  may  be  indicated  by  the 
presence  of  a  murmur. 

Furthermore,  the  condition  of  the  pulse  and  the  size  of  the  liver 
should  be  ascertained.  The  absence  of  any  abnormality  in  both 
of  these  respects  would  strongly  contra-indicate  disease  of  the 
heart. 

The  site  of  production  and  direction  of  transmission  of  the 
murmur,  together  with  its  character  and  rhythm,  would  afford  valu- 
able and,  in  many  instances,  unmistakable  evidence  in  favour  of  its 
endocardial  or  exocardial  origin.  It  is  not  necessary  here  to  repeat 
the  points  which  are  of  diagnostic  value.  The  lungs  should  be 
examined  in  all  cases  in  which  a  murmur  of  doubtful  significance 
is  heard,  and  the  effect  of  the  respiratory  movements  and  of  holding 
the  breath  on  the  abnormal  sound  should  be  carefully  observed. 
A  murmur  of  equivocal  import  in  cases  of  tubercular  disease  of  the 
upper  lobe  of  the  left  lung  would  favour  an  exocardial  origin,  in 
view  of  the  rarity  with  which  endocardial  changes  occur  in  phthisis. 
Congestion  of  the  bases  of  the  lungs  with  a  systolic  apical  murmur 
would  strongly  suggest  a  valvular  lesion. 


METHODS   OF   DIAGNOSIS  71 

The  effect  of  changes  in  position  on  the  murmur  sometimes 
affords  very  valuable  information.  A  bruit  which  disappears  when 
the  patient  lies  down  is  almost  certainly  produced  outside  the 
heart. 

C.    VASCULAR  SOUNDS 

1.  Normal  sounds. — It  has  already  been  mentioned  that  under 
normal  conditions  the  second  sound  of  the  heart  is  audible  in  the 
neck  over  the  carotid  and  subclavian  arteries.  It  is  conducted 
thither  by  the  walls  of  the  vessels  and  the  contained  column  ot 
blood  which  intervene  between  the  heart  and  the  site  of  audibility 
of  the  sound. 

If  the  stethoscope  be  placed  lightly  over  the  carotid,  subclavian, 
or  even  femoral  arteries  a  dull  sound  or  thud  may  be  heard  corre- 
sponding with  the  ventricular  systole.  It  has  been  thought  that, 
at  all  events  in  the  case  of  the  carotid  and  subclavian  arteries,  this 
thud  may  be  the  first  sound  of  the  heart  conducted  along  the  walls 
of  the  intervening  vessels.  The  sound  is,  however,  in  all  proba- 
bility of  local  origin,  and  is  caused  by  the  pressure  of  the 
stethoscope,  and  this  is  still  more  likely  in  the  case  of  the  femoral 
arteries. 

Whatever  be  the  explanation  of  the  foregoing  phenomenon,  it  is 
found  that  when  a  certain  moderate  degree  of  pressure  is  made 
with  the  stethoscope  over  the  vessels  in  question,  the  sound  just 
referred  to  is  replaced  by  a  murmur  synchronous  with  the  systole 
of  the  heart.  It  may  be  remarked,  however,  that  this  disposition 
of  events  is  not  always  easy  to  obtain.  The  murmur  is  most 
probably  due  to  a  local  narrowing  of  the  vessel  caused  by  the 
pressure  of  the  stethoscope,  whereby  the  conditions  for  the  forma- 
tion of  a  fluid  vein  are  produced.  A  continuous  murmur,  audible 
over  the  internal  jugular  vein  at  the  root  of  the  neck,  is  explained 
in  a  similar  way,  and  is  observed  under  perfectly  healthy  conditions. 

It  is  said  that  a  "  to  and  fro  "  murmur,  i.e.  systolic  and  diastolic, 
may  be  heard  over  the  femoral  artery  under  normal  conditions,  but 
the  statement  is  open  to  serious  doubt.  The  question  will  be 
referred  to  again  under  the  next  heading. 

2.  Adventitious  sounds.  Arterial. —  Systolic  and  diastolic 
murmurs  produced  at  the  aortic  orifice  may  be  conducted  some 
distance  along  the  great  arterial  trunks,  and  are  commonly  to  be 
heard  in  the  neck.  It  is  said  that  a  shrill  diastolic  murmur  of  aortic 
origin  may  be  audible  over  the  radial  artery  at  the  wrist. 

In  cases  of  aortic  regurgitation  a  combined  systolic  and  diastolic 
murmur  may  be  heard  over  the  femoral  artery. 

The  method  of  production  of  the  systolic  portion  has  already 
been  considered.  The  diastolic  moiety  depends  on  a  similar 
mechanism.  Thus,  in  consequence  of  the  incompetence  of  the 
aortic  valve,   there  is  a  general  reflux  of  blood  towards  the  left 


J2  DISEASES   OF   THE    HEART 

ventricle  during  diastole.  As  the  current  of  blood  flows  backwards 
past  the  constriction  in  the  femoral  artery,  produced  by  the  pressure 
of  the  stethoscope,  a  fluid  vein  is  formed,  and  hence  a  murmur. 
The  diastolic  part  of  the  combined  murmur  is  shorter  and  fainter 
than  the  systolic  portion 

Under  normal  conditions  the  presence  of  a  diastolic  murmur 
over  the  femoral  artery  is  explained  by  the  supposition  of  a  high 
degree  of  dicrotism  of  the  pulse. 

A  systolic  murmur  audible  over  the  subclavian  arteries  above 
and  below  the  clavicles,  and  most  marked  on  the  left  side,  still 
remains  to  be  mentioned.  The  murmur  is  modified  by  the 
respiratory  movements,  and  may  be  annulled  or  intensified  by 
taking  a  deep  breath.  Its  mode  of  production  is  still  a  matter 
of  doubt. 

A  systolic  bruit  is  occasionally  heard  over  the  arteries  in  the 
neck  in  cases  of  anaemia. 

Aneu7-isvial. — The  sounds  which  may  be  heard  over  an  aneurismal 
sac  in  the  neighbourhood  of  the  heart  are  very  variable.  Most 
commonly  two  sounds,  corresponding  with  those  of  the  heart,  are 
observed.  The  second  sound  is  accentuated  and  of  a  lower  pitch 
than  normal,  and  it  may  be  preceded  by  a  systoHc  murmur.  The 
first  sound  may  be  absent,  and  a  systolic  bruit,  followed  by  a  second 
sound,  may  alone  be  audible.  In  other  instances  a  systoHc  and 
diastolic  murmur  are  heard  while  the  sounds  of  the  heart  are 
absent. 

The  systolic  murmur  may  be  conducted  from  the  aortic  orifice,  or 
it  may  be  produced  at  the  mouth  of  the  aneurism.  The  diastolic 
murmur  is  probably  always  conducted  from  the  aortic  opening. 

Venous. — A  continuous  murmur,  the  "  bruit  de  diable,"  may  be 
heard  over  the  internal  jugular  veins  at  the  root  of  the  neck  in  cases 
of  anaemia.  The  bruit  is,  however,  not  peculiar  to  anaemia.  It 
may  occur  under  perfectly  healthy  conditions,  and  it  has  been 
observed  in  50  per  cent,  of  cases  showing  no  signs  of  antemia. 

The  murmur,  which  has  a  musical  humming  quality,  is  usually 
most  distinct  on  the  right  side.  The  intensity  of  the  murmur  is 
increased  by  the  upright  position,  by  turning  the  head  away  from  the 
side  that  is  being  auscultated,  and  by  a  deep  inspiration.  It  is  also 
greatly  modified  by  the  degree  of  pressure  exercised  by  the  stetho- 
scope over  the  vessel.  The  intensity  of  the  murmur  is  also  increased 
during  inspiration  and  during  auricular  diastole. 

The  murmur  has  been  ascribed  to  the  alteration  in  the  calibre 
of  the  vein  produced  by  the  pressure  of  the  stethoscope  and 
the  consequent  production  of  a  fluid  vein.  In  many  cases,  how- 
ever, it  may  be  heard  when  the  instrument  is  placed  over  the 
sternoclavicular  joint,  where  no  pressure  on  the  soft  parts  is 
possible. 

It  is  probable  that  the  anatomical  relations  of  the  lower  part  of 


METHODS  OF  DIx^GNOSIS  73 

the   internal   jugular   veins    exert   an    important    influence    on    the 
production  of  the  murmur. 

This  portion  of  the  vessel  is  intimately  connected  with  the  cervical 
fascia,  so  that  its  calibre  remains  constant. 

If,  now,  the  dimensions  of  the  vein  above  or  below  this  site  are 
diminished,  or  increased,  respectively,  the  adherent  portion  of  the 
vessel  becomes  relatively  dilated,  or  constricted,  as  the  case  may  be, 
and  these  are  the  conditions  for  the  formation  of  a  fluid  vein. 

According  to  some  writers  a  general  contraction  of  the  veins  on  a 
diminished  quantity  of  blood  in  circulation  is  present  in  anaemia, 
while  others  suppose  that  these  structures  undergo  relaxation  from 
malnutrition  and  loss  of  tone.  In  either  event  the  theory  advanced 
above  will  explain  the  presence  of  a  murmur  over  the  internal 
jugular  vein. 

In  some  instances  the  adherent  portion  of  the  vein  is  normally 
somewhat  pouched,  and  it  may  be  that  an  alteration  in  the  quality 
of  the  blood  would,  under  these  conditions,  be  sufficient  to  deter- 
mine the  formation  of  a  fluid  vein.  It  must  be  borne  in  mind,  too, 
that  diminished  viscosity  of  the  blood,  and  lessened  peripheral 
resistance,  play  an  important  part  in  the  production  of  hjemic 
murmurs. 

A  venous  hum  is  not  present  in  all  cases  of  ansemia,  and  the 
intensity  of  the  murmur  does  not  necessarily  correspond  with  the 
degree  of  deterioration  in  the  quality  of  the  blood. 

A  bruit  may  also  be  heard  over  the  longitudinal  and  lateral 
sinuses,  and  over  the  subclavian  and  other  veins  in  cases  of 
anaemia. 

A  continuous  venous  murmur,  apart  from  ansmia,  is  occasionally 
heard  on  either  side  of  the  xiphoid  cartilage,  and  has  been  ascribed 
to  constriction  of  the  inferior  vena  cava  at  its  junction  with  the 
right  auricle. 

The  murmur  resembles  the  fitful  blowing  of  wind  through  the 
rigging  of  a  ship  under  bare  poles. 

In  those  exceedingly  rare  instances  in  which  a  communication  is 
formed  between  the  ascending  aorta  and  superior  vena  cava,  a 
murmur  may  be  heard  over  the  first  or  second  right  intercostal  space 
an  inch  or  more  from  the  sternal  edge,  which  bears  a  resemblance  to 
the  sound  produced  by  a  water-wheel  in  motion. 

The  continuous  murmur  which  attends  the  establishment  of  a 
communication  between  the  aorta  and  pulmonary  artery,  a  very  rare 
event,  is  heard  best  close  to  the  left  sternal  edge,  about  the  level  of 
the  second  costal  cartilage.  The  murmur  heard  under  these 
circumstances,  though  continuous,  is  not  uniform  in  intensity,  but 
varies  rhythmically  with  the  balance  of  pressure  in  the  two  vessels. 


CHAPTER    IV 
THE    PULSE 

Definition — Method  of  Production — Physical  Examination  of  Pulse — Inspection 
— Palpation — Graphic  Record  or  Sphygmogram — Instrumental 
Determination  of  the  Blood  Pressure. 

From  a  clinical  point  of  view  the  pulse  is  the  alteration  in  the  shape 
of  an  artery  which  obtains  during  the  time  that  each  wave  of 
increased  pressure,  due  to  the  heart's  systole,  passes  along  the 
vessel.  The  perception  of  the  pulse  rests  on  the  visible  and  palp- 
able displacement  which  the  artery  imparts  to  the  media  in  con- 
tact with  it,  as  each  wave  of  increased  pressure  passes  beneath  the 
point  of  contact. 

The  pulse  depends  on — 

1.  An  alteration  in  the  shape  of  the  artery  from  the  flattened  to 

the  cylindrical  (Broadbent). 

2.  A  shght  expansion  of  the  artery. 

An  artery  is  usually  flattened  by  the  tissues  which  overlie  it,  and 
exercise  pressure  against  some  underlying  and  resistant  medium. 
In  the  case  of  the  radial  artery  it  is  the  radius  against  which  the 
vessel  is  pressed.  The  artery  is  still  further  flattened  by  the 
examining  finger.  All  elastic  tubes,  however,  tend  to  become 
circular  when  the  fluid  pressure  w'ithin  them  is  sufficient  to  over- 
come the  resistances  which  conduce  to  alterations  in  their  shape. 
Thus  it  is  that  as  the  pulse  wave  passes  any  particular  point  in  the 
course  of  an  artery,  the  vessel's  shape  is  altered  from  the  flattened 
to  the  circular,  and  a  false  impression  of  expansion  is  experienced. 
In  addition  to  this  factor  in  the  production  of  the  pulse  the  arterial 
wall  does  actually  expand,  but,  in  the  case  of  the  radial  artery,  to 
an  extent  which  could  scarcely  be  appreciated  by  the  finger. 

The  physical  examination  of  the  pulse  includes — 

1.  Inspection 

2.  Palpation 

3.  Graphic  record  or  sphygmogram 

4.  The   instrumental   determination    of   the   blood 

pressure. 

74 


THE   PULSE  75 

INSPECTION. 

The  information  derived  from  inspection  of  the  pulse  is  always 
checked  by  subsequent  palpation.  Nevertheless  this  method  of 
investigation  has  its  value  as  a  means  of  rapid  diagnosis.  The 
vessels  which  lend  themselves  most  readily  to  this  mode  of  examina- 
tion are  the  temporal  arteries,  and  occasionally  the  retinal  arteries, 
since  the  course  of  these  vessels  can  usually  be  seen  in  the  adult  by 
careful  inspection.  The  degree  of  tortuosity  of  the  artery,  and  the 
frequency,  regularity,  and  to  some  extent  the  character  of  the  pulse, 
as  well  as  the  bilateral  symmetry  of  the  pulsation,  can  be  roughly 
gauged.  Thus  aortic  regurgitation  may  be  suspected  in  cases  where 
the  discursion  of  the  pulse  is  extensive,  the  collapse  of  the  pulse 
wave  sudden,  and  the  vessels  tortuous.  Heart  failure,  especially  in 
mitral  regurgitation,  is  suggested  by  inequalities  in  the  force  and 
rhythm  of  the  visible  pulse.  Visible  pulsation  of  the  carotid  arteries 
is  frequently  associated  with  aortic  regurgitation,  and  also  with  ex- 
ophthalmic goitre  and  other  nervous  disorders  of  the  heart.  Other 
points,  which  may  be  observed  on  inspection,  have  their  diagnostic 
value  as  described  under  palpation  of  the  pulse. 

PALPATION 
Method  of  Feeling  the  Pulse 

The  first  three  fingers  should  be  placed  lightly  upon  the  radial  artery 
at  the  wrist,  with  the  forefinger  nearest  the  heart  and  the  thumb 
supporting  the  wrist.  The  vessel  should  be  investigated,  under 
varying  degrees  of  pressure,  both  in  its  transverse  and  longitudinal 
aspects,  and  each  feature  of  the  pulse  that  requires  attention  should 
be  appreciated  by  a  distinct  and  well-defined  manoeuvre  of  the 
examining  fingers. 

The  features  of  the  pulse  to  which  the  observer's  attention  should 
be  directed  are  the  following  :■ — • 

1.  The  frequency.     While  counting  the  pulse  rate,  the  regularity 

or  irregularity  of  the  force  and  rhythm  of  the  pulse  should 
also  be  observed. 

2.  The  size  of  the  artery. 

3.  The  degree  of  fulness  of  the  artery  between  the  pulsations. 

4.  The  character  of  the  pulse  wave. 

5.  The  compressibility  of  the  vessel. 

6.  The  condition  of  the  arterial  wall. 

7.  The  bilateral  symmetry  of  the  pulsations. 

I.  The  freoLuency  of  the  pulse. — The  rate  of  the  pulse  and  of  the 
heart  beats  usually  correspond  ;  but  this  is  not  always  the  case,  inas- 
much as  the  force  of  the  cardiac  systole  may  not  be  suflicient  to 
propel  the  pulse  wave  as  far  as  the  radial  artery.     The  average 


76  DISEASES   OF   THE   HEART 

rate  of  the  pulse  in  the  adult  male  is  about  seventy-two  beats 
per  minute. 

The  conditions  which  give  rise  to  physiological  variations  in  the 
frequency  of  the  pulse  are  :  (i)  Age,  i.e.  the  pulse  rate  is  quicker 
in  children  than  in  adults;  (2)  Sex,  i.e.  the  pulse  rate  is  quicker 
in  women  than  men ;  (3)  Heredity ;  (4)  Nervous  impressions ; 
(5)  Emotional  disturbance;  (6)  Exertion;  (7)  Position;  (8)  Food; 
(9)  Temperature;  (10)  Time  of  day  or  night;  (11)  Alterations  in 
blood  pressure,  etc. 

The  pulse  rate  is  also  influenced  by  drugs,  such  as  alcohol, 
tobacco,  digitalis,  and  the  like. 

The  variations  in  the  pulse  rate  produced  by  disease  may  be 
tabulated  as  follow  : — 

A.  Increased  Frequency  of  the  Pulse 
(i)  Pyrexia.  (2)  Ansemia.  (3)  Pathological  conditions  which 
decrease  blood  pressure.  (4)  Pericarditis.  (5)  Myocarditis. 
(6)  Valvular  disease  of  the  heart.  (7)  Dilatation  of  the  heart. 
(8)  Irritable  heart  (Da  Costa).  (9)  Loss  of  vagus  control,  or 
irritation  of  the  cervical  sympathetic  (accelerator)  nerves  as 
observed  in  cases  of  palpitation,  ex-ophthalmic  goitre,  etc, 
(10)  Tachycardia.     (11)  Hysteria. 

B.  Diminished  Frequency  of  the  Pulse 
(i)  Renal  disease.     (2)   Pathological  conditions  which  increase 
blood  pressure.     (3)  Jaundice.     (4)  Fatty  and  occasionally 
fibroid   disease   of   the   heart    (the  pulse   rate   is,   however, 
sometimes  increased  under  these  circumstances).     (5)  Epi- 
lepsy and  other  cerebral  disorders.     (6)  Pain.     (7)  During 
convalescence  from   the  acute  fevers,   such  as  pneumonia, 
typhoid,  etc. 
The  diminished  frequency  of  the  pulse  that  is  found  in  association 
with  the  remarkable  condition  in  which  two  beats  of  the  heart  occur 
to  one  of  the  pulse  is  of  course  not  included  in  the  present  category. 
The  condition  is  mentioned  here  with  the  object  of  emphasizing  the 
necessity  of  controlling  observations  made  with  respect  to  the  fre- 
quency of  the  pulse  at  the  wrist  by  an  examination  of  the  heart. 

Rhythm 

The  rhythm  of  the  pulse  and  of  the  heart's  action  usually  corre- 
spond, but,  as  in  the  condition  just  mentioned,  this  is  not  necessarily 
the  case. 

Deviations  from  the  normal  rhythm  give  rise  either  to  "inter- 
mittence"  or  to  "irregularity"  of  the  pulse,  or  to  a  combination  of 
these  conditions. 

Intermittence  of  the  pulse  means  the  omission  of  a  beat,  which 
may  occur  at  regular  or  irregular  intervals.  The  phenomenon  is 
more  commonly  observed  in  old  than  in  young  people,  and  it  is  fre- 


THE  PULSE 


77 


quently  found  independent  of  any  other  discoverable  abnormality. 
It  is  habitual  in  some  individuals,  while  in  others  it  is  readily  pro- 
duced by  emotional  disturbance,  indigestion,  or  the  abuse  of  tea  and 
tobacco.  Intermittence  of  the  pulse  is  also  observed  in  association 
with  gouty  manifestations.  It  is  sometimes  found  in  connection  with 
fatty  disease  of  the  heart,  with  cardiac  failure,  and  with  acute  affections 
of  the  lungs,  and  is  then  of  serious  import.  It  is  said  that  habitual 
intermittence  of  the  pulse  usually  disappears  during  attacks  of  pyrexia. 

Irregularity  of  the  pulse  usually,  but  not  necessarily,  implies  in- 
equalities in  the  force  and  volume  of  the  pulsations,  as  well  as  the 
appearance  of  the  beats  at  unequal  intervals  of  time.  It  is  asso- 
ciated with  valvular  disease  of  the  heart,  and  more  especially  with 
mitral  regurgitation.  It  is  also  commonly  observed  in  connection 
with  failure  of  the  heart  from  any  cause,  and  speaking  generally,  it  is 
a  sign  of  disturbance  of  myocardial  metabohsm.  Irregularity  of  the 
pulse  sometimes  depends  on  reflex  disturbance  of  the  heart  from 
gastro-intestinal  and  uterine  disorders.  It  also  occurs  in  association 
with  the  abuse  of  tea,  coffee,  and  tobacco.  It  is  occasionally  found 
apart  from  any  other  morbid  manifestations. 

Certain  peculiar  modifications  in  the  rhythm  of  the  pulse  are 
designated  under  the  special  titles  of  the  pulsus  bigeminus,  the 
pulsus  trigeminus,  the  pulsus  alternans,  and  the  pulsus  paradoxus. 

Pulsus  bigeminus. — In  this  variety  of  pulse  the  beats  are  grouped 
in  pairs,  with  a  pause  between  each  group.  The  second  beat  is 
usually  the  weaker  of  the  two.  The  heart  beats  correspond  in 
rhythm  with  the  pulse,  so  that  a  strong  impulse  is  followed  by  a 
weak  one.  This  variety  of  pulse  is  found  most  commonly  in  mitral 
stenosis,  more  especially  when  under  the  influence  of  digitalis.  It 
is  also  observed  in  association  with  bodily  and  mental  strain  and 
with  epileptiform  attacks. 

Pulsus  trigeminus. — In  this  variety  of  pulse  the  beats  are  arranged 
in  groups  of  three.  It  occurs  under  conditions  similar  to  those 
in  which  the  pulsus  bigeminus  is  observed. 

Pulsus  alterfians — The  regular  succession  of  a  strong  and  weak 
pulsation  constitutes  the  pulsus  alternans,  which  is  observed  in 
connection  with  Cheyne-Stokes'  respiration,  (Sansom)  and  with  the 
other  conditions  of  central  nervous  disturbance,  and  occasionally 
also  with  mitral  affections. 

Pulsus  paradoxus. — In  this  condition  the  pulse  is  markedly 
influenced  by  the  respiratory  movements.  During  inspiration  the 
pulse  wave  is  annulled,  or  becomes  much  diminished  in  force, 
while  during  expiration  it  may  be  of  full  amplitude.  It  can  some- 
times be  elicited  under  physiological  conditions  by  holding  the 
breath  in  extreme  inspiration  or  expiration.  In  certain  pathological 
conditions,  however,  it  is  more  or  less  constantly  present.  It  occurs 
in  association  with  pericardial  adhesions,  mitral  stenosis,  emphy- 
sema, and  with  conditions  of  heart  failure. 


y8  DISEASES    OF   THE    HEART 

So  far  as  the  mechanism  of  production  of  this  variety  of  pulse 
is  concerned,  it  is  probable  that  the  increase  of  negative  pressure  in 
the  thorax  with  each  inspiration  offers  a  greater  resistance  to  the 
discharge  of  the  ventricular  contents  than  an  enfeebled  heart  is  able 
to  cope  with. 

The  pulsus  paradoxus  is  of  small  diagnostic  value. 

2.  The  size  of  the  artery. — Observations  on  this  head  are  of 
importance,  inasmuch  as  the  size  of  the  artery  appreciably  affects 
the  perception  of  the  size  and  force  of  the  pulse  wave.  Thus  the 
pulse  wave  in  a  large  artery  will  appear  more  forcible  than  in  a 
small  one,  but,  on  the  other  hand,  the  pulsation  is  much  more 
easily  obliterated  by  pressure  with  the  fingers  in  the  former  case  than 
in  the  latter.  The  size  of  the  artery,  therefore,  becomes  one  of  the 
factors  in  the  estimation  of  the  strength  or  force  of  the  pulse. 

The  size  of  the  artery  depends  for  the  most  part  on  the  condition 
of  contraction  or  relaxation  of  the  vessel,  which  is  of  course  regulated 
by  the  tone  of  the  arterial  walls.  The  thickness  of  the  arterial  wall 
also  effects  to  a  slight  extent  the  size  of  the  vessel. 

The  size  (calibre)  of  the  artery  is  most  accurately  determined  by 
means  of  Oliver's  arteriometer. 

The  systematic  use  of  this  instrument  is  of  very  great  service, 
inasmuch  as  it  enables  a  record  to  be  kept  of  the  calibre  of  the 
artery  for  purposes  of  comparison  and  reference. 

3.  The  degree  of  fulness  of  the  artery  between  the  pulsations. — 
The  degree  of  fulness  of  the  artery  between  the  beats  of  the  pulse  is 
the  measure  of  the  mean  intra-arterial  pressure,  or  pulse  tension, 
and  is  determined  by  (i)  the  force  of  the  ventricular  systole,  (2)  the 
peripheral  resistance,  and  (3)  the  competency  of  the  aortic  valve. 

In  order  to  determine  the  tension  of  the  pulse  the' fingers  should 
be  carried  transversely  to  and  fro  across  the  artery,  and  an  attempt 
made  to  roll  the  vessel  beneath  the  fingers. 

When  the  artery  can  be  felt  distinctly  during  the  passage  of  the 
pulse  wave  beneath  the  finger,  and  is,  with  care,  distinguishable 
between  the  pulsations,  the  pulse  may  be  regarded  to  be  of  average 
tension.  When  the  artery  cannot  be  clearly  outlined  by  the  fingers 
at  any  period  of  the  passage  of  the  pulse  wave,  or  during  the  interval 
between  the  pulsations,  the  pulse  is  said  to  exhibit  low  tension. 
AVhen  the  artery  can  be  rolled  beneath  the  fingers  during  and 
between  the  pulsations  the  pulse  is  described  as  one  of  high  tension. 
An  artery  that  is  empty  between  the  beats  of  the  pulse  (low- 
tension  pulse)  depends  on  a  general  want  of  tone  of  the  ventricular 
and  arterial  walls,  and  is  occasioned  by — 

(i;  Pyrexia.  (2)  Hereditary  influences.  (3)  General  debility,  due 
to  anxiety  or  nervous  strain  of  any  kind,  excesses  of  various 
kinds,  bad  hygienic  surroundings,  ansemia,  and  so  forth. 
(4)  Food.  (5)  Serious  purgation.  (6)  Exhaustion  or  fatigue 
from  any  cause.  (7)  Fatty  degeneration  of  the  heart.  (8) 
Dilatation  of  the  heart.  (9)  Aortic  regurgitation.  (10)  Mitral 
regurgitation,  etc. 


THE   PULSE  79 

An  artery  that  is  full  between  the  beats  of  the  pulse  (high-tension 
pulse)  depends  on  (i)  increase  in  the  quantity  of  blood  in  the 
circulation,  (2)  forcible  action  of  the  heart,  (3)  increased  arterial 
tone  and  arterio-capillary  resistance,  and  is  occasioned  by — 

(i)  Age.  (2)  Hereditary  influences.  (3)  Renal  disease.  (4)  Gout. 
(5)  Pregnancy.  (6)  Lead  poisoning.  (7)  Aneemia  (in  some 
cases).  (8)  Diabetes  (in  some  cases).  (9)  An  attack  of 
angina  pectoris.  (10)  Constipation.  (11)  Peritonitis.  (12) 
Emphysema  and  chronic  bronchitis.  (13)  Aortic  and  mitral 
stenosis,  etc. 

4.  The  character  of  the  pulse  wave. — The  character  of  the  pulse 
wave  must  be  considered  with  regard  to  its  rise,  duration,  and  fall. 
The  rise  of  the  pulse  wave  may  be  sudden  or  gradual,  of  great 
or  of  small  amplitude. 

It  is  sudden  and  of  great  amplitude  when  a  comparatively  large 
amount  of  blood  is  pumped  into  an  empty  arterial  system,  as  in 
(r)  aortic  regurgitation  with  hypertrophy  of  the  heart,  (2)  after 
hsemorrhage,  (3)  in  most  pulses  of  low  tension.  The  rise  of  the 
pulse  wave  is  gradual  if  the  ventricle  can  empty  itself  slowly  only  into 
the  aorta,  as  in  (i)  aortic  stenosis,  (2)  aneurism  of  the  aorta,  (3) 
high-tension  pulses. 

The  rise  of  the  pulse  wave  is  of  small  amplitude  (i)  when  the 
pulse  tension  is  high,  (2)  when  the  amount  of  blood  ejected  into 
the  aorta  is  small,  as  in  mitral  stenosis,  mitral  regurgitation,  etc. 

The  duration  of  the  pulse  wave  is  considerable  when  the  pulse 
tension  is  high  and  the  ventricular  systole  powerful,  as  in  cases 
of  high  tension,  aortic  stenosis,  etc. 

The  duration  of  the  pulse  wave  is  short  when  the  pulse  tension 
is  low  or  the  ventricular  systole  is  weak,  as  in  low-tension  pulses 
and  failure  of  the  heart,  etc. 

The  fall  of  the  pulse  wave  may  be  sudden  or  gradual,  with  or 
without  subsidiary  pulsations.  A  sudden  fall  of  the  pulse  wave  is 
observed  in  cases  of  (i)  aortic  regurgitation,  (2)  pulses  of  low 
tension. 

A  gradual  fall  of  the  pulse  wave  is  observed  in  (i)  aortic 
stenosis,  (2)  pulses  of  high  tension,  (3)  aneurism. 

Seco7idary  pulsations,  etc.—Hh&  dicrotic  wave  is  practically  the 
only  secondary  or  subsidiary  pulsation  appreciable  to  the  finger. 
It  is  most  commonly  observed  when  the  pulse  tension  is  low  and 
the  heart  beat  forcible.  A  fuller  account  of  the  dicrotic  pulse  and 
of  the  other  subsidiary  waves  that  may  be  observed  will  be  given 
under  the  account  of  the  sphygmogram. 

5.  The  compressibility  of  the  artery. — The  strength  of  the  pulse, 
and  the  degree  of  the  constant  or  mean  intra-arterial  pressure  or 
tension,  is  computed  from  the  compressibility  of  the  artery.  The 
degree  of  pressure  that  is  required  to  obliterate  the  pulse  is  the 
measure  of  its  strength.     The   degree   of  intra-arterial   pressure   is 


8o  DISEASES   OF  THE   HEART 

gauged  by  the  amount  of  force  that  is  required  to  flatten  the  artery 
between  the  pulsations. 

The  method  of  estimating  the  compressibility  of  the  artery  and 
hence  of  the  variable  and  constant  pressure  within  the  vessel  is 
as  follows  :  Three  fingers  are  placed  upon  the  radial  artery  in  the 
manner  previously  described.  The  two  fingers  nearest  the  heart 
exercise  pressure  upon  the  artery  until  the  pulsations  are  obliterated, 
that  is,  they  cannot  be  felt  by  the  third  finger.  The  degree  of 
pressure  that  is  required  to  extinguish  the  pulse  is  the  measure 
of  its  strength.  The  three  fingers  may  be  used  to  compress  the 
vessel  between  the  beats,  and  the  degree  of  pressure  that  is  required 
to  flatten  the  artery  is  the  guide  to  the  estimation  of  the  mean 
arterial  tension. 

The  artery  is  difficult  to  compress  in  (i)  pulses  of  high  tension, 
(2)  when  the  vessel  is  rigid  from  degenerative  changes  in  its  walls. 

The  artery  is  easy  to  compress  in  pulses  of  low  tension. 

6.  The  condition  of  the  arterial  wall. — In  order  to  estimate  the 
condition  of  the  arterial  wall,  the  fingers  should  carry  the  skin  up 
and  down  along  the  course  of  the  vessel  with  varying  degrees  of 
pressure. 

The  healthy  arterial  wall  is  soft  and  elastic  to  the  touch.  On 
passing  the  fingers  along  the  course  of  the  artery  and  applying  some 
pressure,  no  variations  in  consistency,  or  irregularity  in  outUne  should 
be  felt.  If  the  vessel  feels  unnaturally  rigid,  with  irregularities  in 
thickness  and  density,  especially  when  this  is  combined  with  tor- 
tuosity of  outline,  the  arterial  wall  has  undergone  degeneration. 

Hardened  patches  are  due  to  established  or  commencing  cal- 
careous deposition,  and  the  tortuosities  depend  on  the  loss  of 
elasticity  of  the  arterial  coat  in  conjunction  Avith  strain  on  the 
vessel.  In  extreme  cases  the  artery  is  found  to  be  converted  into 
a  rigid  calcareous  tube. 

Atheroma  is  a  frequent  sequel  of  protracted  high  arterial  tension. 
It  is  usually  present  to  a  greater  or  less  degree  in  old  age. 

7.  The  bilateral  symmetry  of  the  pulsations.  —  In  cases  of 
doubtful  nature  it  is  well  to  make  a  practice  of  examining  the 
pulse  at  each  wrist  simultaneously,  with  the  object  of  disclosing 
any  want  of  synchronism,  or  differences  in  the  size  or  character 
of  the  two  pulses  that  may  obtain. 

Apart  from  an  abnormal  distribution  of  the  arteries,  a  want  of 
synchronism,  or  a  marked  difference  in  the  size  or  character  of  the 
two  radial  pulses,  is  usually  indicative  of  aneurism  of  one  or  other 
of  the  great  arterial  trunks. 

Recurrent  pulse. 

This  pulse,  which  is  felt  as  a  feeble  and  retarded  beat  on  the 
distal  side  of  the  radial  artery  after  this  vessel  has  been  completely 
blocked  by  pressure  with  the  fingers,  is  due  to  the  transmission  of  a 


THE   PULSE  8i 

wave  through  the  palmar  arch  by  way  of  the  ulnar  artery.  It  is 
observed  in  cases  of  extremely  low  tension,  with  a  vigorous 
ventricular  contraction,  as,  for  instance,  in  aortic  regurgitation, 
and  also  in  conditions  where  protracted  high  tension  has  led  to 
failure  of  the  muscular  coats  of  the  arteries,  as,  for  example,  may 
obtain  in  the  terminal  stages  of  chronic  Bright's  disease. 


GRAPHIC  RECORD  OR  SPHYGMOGRAM 

For  a  description  of  the  sphygmograph  and  its  method  of  use  the 
reader  is  referred  to  works  on  physiology. 

The  sphygmogram  is  a  tracing  of  the  discursions  of  the  pulse 
magnified  by  the  lever  mechanism  of  the  sphygmograph,  and 
registered  on  a  recording  surface.     It  consists  of — 

1.  An  ascending  Umb  {a-b) 

2.  An  apex  {b) 

3.  A  descending  limb  {b-g),  which  is  interrupted  by  one  or  more 

secondary  waves  and  notches,  viz. — 
I  (a)  The  tidal  or  predicrotic  wave  {d) 

(b)  The  aortic  notch  (e) 
{c)  The  dicrotic  wave  (/) 
{d)  Subsidiary  or  post-dicrotic  waves 


FIG.    14.       NORMAL    PULSE   TRACING 

I.  The  Ascending   Limb 

In  health  this  line  is  vertical,  or  nearly  so.    Its  amplitude  depends 
on — 

1.  The  energy  of  the  heart's  beat 

2.  The  intra-arterial  tension 

3.  The  magnifying  power  of  the  lever  mechanism 

4.  The  skill  of  the  operator 

The   energy   of   the   heart's   beat. — Ceteris  paribus,   the   more 
energetic  the  beat  of  the  heart  the  greater  the  amplitude  of  the 

G 


82  DISEASES   OF   THE   HEART 

ascending  limb  of  the  pulse  trace,  but  owing  to  the  correlslion 
between  the  cardiac  and  vascular  mechanisms,  it  usually  happens 
that  when  the  heart's  beat  is  forcible  the  arterial  tension  is  high. 
Hence  the  effect  of  a  powerful  ventricular  contraction  on  the  ampli- 
tude of  the  ascending  limb  of  the  sphygmogram  is  largely  neutralized. 

The  intra-arterial  tension. — When  the  arterial  tension  is  high  the 
artery  is  circular,  not  only  during  the  passage  of  the  pulse  wave,  but 
also  during  the  interval  between  the  pulsations,  unless  the  vessel  be 
subjected  to  great  pressure.  Hence  the  full  effect  of  the  change 
of  shape  in  the  artery,  i.e.  from  the  flattened  to  the  circular,  loses 
its  due  influence  on  the  percussion  stroke,  which,  in  consequence,  is 
of  low  amplitude.  When,  on  the  other  hand,  the  tension  is  low 
the  artery  is  flattened  between  the  beats  of  the  pulse  by  the  pressure 
of  the  small  arm  of  the  lever  of  the  sphygmograph ;  and  hence  the 
discursion  of  the  long  arm  of  the  lever,  when  the  vessel  becomes 
circular,  is  considerable  or  great  as  the  case  may  be. 

The  skill  of  the  operator. — Unless  the  lever  be  accurately  ad- 
justed over  the  artery,  the  displacement  of  the  tissues  surrounding 
the  vessel,  and  not  that  of  its  walls,  is  imparted  to  the  sphygmo- 
graph. There  is  for  every  degree  of  tension  a  degree  of  pressure 
which  produces  the  maximum  discursion  of  the  lever.  This  can  be 
found  by  experiment  only,  and  by  the  skilled  operator. 

The  ascending  limb  of  the  sphygmogram  is  of  great  amplitude  in — 

1.  Aortic  regurgitation 

2.  Pulses  of  low  tension  with  forcible  heart  beat 

3.  The  pulse  after  haemorrhage 

The  ascending  limb  is  of  small  amplitude  in — 

1.  Pulses  of  high  tension 

2.  Mitral  disease 

3.  Aortic  stenosis 

4.  Aneurism 

2.  The  Apex  {b) 

The  apex  is  the  angle  included  between  the  ascending  and 
descending  Umbs  of  the  sphygmogram.  It  is  normally  acute.  Its 
arc,  however,  largely  depends  on  the  rate  of  movement  of  the 
recording  surface. 

The  angle  is  very  acute  under  those  conditions  which  produce 
an  ascending  Hmb  of  great  ampUtude.  It  is  obtuse  when  the 
arterial  tension  is  high,  or  when  the  aorta  is  slowly  filled,  as  in 
aortic  stenosis,  and  aneurism  of  the  arch  of  the  aorta.  Sometimes 
the  tracing  has  a  double  apex  {pulsus  bisferietis) — a  condition  which 
sometimes  obtains  in  aortic  stenosis  and  in  cases  of  senile  degenera- 


THE   PULSE 


83 


tion  of  the  arteries.     It  is  compounded  of  two  distinct  efforts  on  the 
part  of  the  ventricle  to  empty  itself. 

3.  The  Descending  Limb  {b-g) 

The  first  part  of  this  line  (b-e)  is  due  to  the  fall  of  the  lever  after 
its  initial  elevation  by  the  pulse  wave.  Together  with  the  ascending 
limb  and  the  apex  it  forms  the  so-called  percussion  wave. 

Tidal  Wave  [D) 

The  explanation  of  the  cause  and  significance  of  the  tidal  wave 
is  most  succinctly  and  clearly  given  by  Mahomed  in  the  following 
words : — 


1. 


2. 


FIG.    15.      MAHOMED  S   SCHEME   OF   THE   TIDAL  WAVE 


"The  simplest  pulsatile  movement  that  can  be  conceived  in  an 
elastic  tube  is  the  mere  passage  of  a  wave  of  fluid  through  it, 
causing  more  or  less  sudden  expansion  and  a  gradual  collapse 
of  the  tube  as  it  passes  through  it;  such  a  wave  is  the  foundation 
of  the  pulse,  and  has  been  called  the  '  Tidal '  wave.  If  the  impulse 
imparted  to  the  fluid  is  more  sudden,  an  element  of  percussion  or 
shock  will  be  introduced  (Fig.  2),  giving  an  abrupt  and  vertical 
up-stroke  from  the  jerking  of  the  lever  by  the  sudden  expansion 
of  the  artery  [change  of  shape. — Author].  Owing  to  its  acquired 
velocity,  this  movement  of  the  lever  is  rather  greater  than  the  corre- 
sponding movement  in  the  arterial  wall  which  produced  it,  and  on 
reaching  its  highest  point,  it  falls  suddenly  by  its  own  weight,  till  it 


84  DISEASES   OF   THE    HEART 

is  again  caught  and  perhaps  slightly  raised  by  the  tidal  wave  B, 
which  is  now  only  reaching  its  maximum  of   distension. 

"...  The  tidal  wave  is  the  true  pulse  wave,  and  indicates  the 
passage  of  a  volume  of  blood  through  the  arteries,  pumped  into 
them  by  each  contraction  of  the  heart.  It  resembles  the  passage 
of  the  tidal  wave  or  '  bore '  up  a  river ;  hence  its  name.  It  is 
transmitted  more  slowly  than  the  percussion  wave,  or  rather  attains 
its  maximum  intensity  more  gradually ;  hence  their  separation  in  the 
tracing.  Though  they  usually  commence  to  distend  the  artery 
together,  the  percussion  wave  necessarily  attains  its  maximum 
intensity  instantaneously,  it  being  only  a  shock,  while  the  tidal 
wave  does  so  more  gradually.  Sometimes  a  considerable  interval 
elapses  between  them.  Frequently  they  are  inseparable,  the  per- 
cussion wave  not  existing  or  else  being  merged  into  the  tidal." 

The  tidal  wave  has  been  explained  on  the  assumption  that  it  is  a 
reflection  of  the  primary  wave  from  the  periphery,  but  the  view  ad- 
vanced above  is  perhaps  the  one  most  commonly  held. 

Aortic  Notch  and  Dicrotic  Wave  {e  and  f) 

The  recoil  of  the  elastic  arterial  walls,  which  follows  their  dis- 
tension by  the  percussion  and  tidal  waves,  forces  the  blood  back-, 
wards  and  forwards  towards  the  aortic  cusps  and  towards  the 
periphery.  The  flow  backwards  closes  the  aortic  valve  (represented 
by  the  aortic  notch),  and  the  barrier  thus  thrown  in  the  path  of  the 
blood  stream  gives  rise  to  a  reflected  wave  of  increased  pressure 
(the  dicrotic  wave).  Other  views  are  held  with  regard  to  the 
causation  of  the  dicrotic  wave,  but  the  explanation  given  here  is 
the  one  most  commonly  accepted. 

The  subsidiary  waves  which  sometimes  appear  on  the  descending 
limb  of  the  sphygmogram  below  the  dicrotic  wave  are  echoes 
of  the  dicrotic  wave.  They  are  due  to  the  vibrations  set  up  in 
the  elastic  arterial  walls  consequent  on  the  injection  of  the  mass 
of  blood  into  the  aorta  at  each  systole  of  the  heart.  As  equilibrium 
is  established  they  gradually  die  away.  Irregular  undulations  on 
the  descending  limb  of  the  pulse  trace  are  sometimes  due  to  vibra- 
tions of  the  sphygmographic  lever,  or  of  the  tissues  in  the  imme- 
diate neighbourhood  of  the  pulse. 

The  application  of  the  foregoing  methods  of  examination  of  the 
pulse  will  now  be  illustrated  in  the  following  brief  description  of  the 
characteristic  features  of  the  pulse  in — 

1.  High  tension 

2.  Low  tension 

3.  Virtual  tension 

4.  Hypertrophy  of  the  heart 

5.  Dilatation  of  the  heart 

6.  Aortic  regurgitation 

7.  Aortic  stenosis 


THE   PULSE  8s 

8.  Combined  aortic  regurgitation  and  stenosis 

9.  Mitral  regurgitation 

10.  Mitral  stenosis 

11.  Combined  mitral  regurgitation  and  stenosis 

12.  Combined  aortic  and  mitral  disease 

13.  Aneurism  of  the  arch  of  the  aorta 

I.    High-tension  Pulse 

Inspection. — Unless  its  walls  are  degenerated  the  vessel  is  usually 
small  and  contracted.  If  degenerated,  the  temporal  arteries  stand 
out  as  thick  sinuous  cords.  The  radial  artery,  under  these  circum- 
stances, is  visible  far  up  the  arm,  and  the  vessel  is  thrown  into 
curves  with  each  pulsation.  The  diameter  of  the  artery  does  not 
appear  to  be  appreciably  altered  during  the  passage  of  the  pulse 
wave. 

Palpation. — The  pulse  is  decreased  in  frequency,  but  regular  in 
force  and  rhythm.  The  vessel  is  small  if  healthy;  large  if  de- 
generated, full  between  the  beats  and  not  easily  compressible.  The 
pulse  wave  is  of  low  amplitude,  rises  slowly,  lasts  long,  falls  slowly, 


FIG.    16.       HIGH-TENSION    PULSE   TRACING 

and  is  difficult  to  compress.     The  arterial  wall,  usually  more  or  less 
thickened,  is  sometimes  extremely  degenerated. 

Sphygmogram. — The  ascending  limb  is  of  low  amplitude,  and 
shows  a  gradual,  somewhat  slanting  ascent.  The  percussion  wave 
is  badly  defined  and  often  absent.  The  apex  (tidal  wave)  is  rounded. 
The  dicrotic  wave  is  small,  and  situated  high  up  on  the  descending 
limb.  The  descending  limb  falls  gradually,  and  is  interrupted  by 
numerous  subsidiary  waves. 

2.   Low-tension  Pulse 

Inspection. — The  pulse  is  often  visible  as  an  energetic  throb. 
The  vessel  cannot  be  seen  between  the  beats. 

Palpation. — The  pulse  is  increased  in  frequency,  but  regular  in 
force  and  rhythm.     The  artery,  which  may  be  large  or  small,  cannot 


86  DISEASES   OF   THE    HEART 

be  felt  between  the  beats.  The  pulse  wave,  which  may  be  of  great 
or  small  amplitude,  in  accordance  with  the  force  of  the  ventricular 
contraction,  rises  quickly,  is  of  brief  duration,  falls  quickly,  and  is 
easily  obliterated  by  pressure. 

Dicrotism  is  always  well  marked,  so  that  in  some  instances  two 
distinct  pulsations  can  be  felt  with  each  beat  of  the  heart.  This 
variety  of  low-tension  pulse  has  been  termed  the  dicrotic  pulse. 

The  arterial  wall  is  healthy. 

Sphygmogram. — The  ascending  limb  rises  quickly,  and  is  of  great 
or  low  amplitude  according  as  the  left  ventricle  is  acting  powerfully 
or  feebly.     The  apex  is  acute  and  the  tidal  wave  badly  marked. 


FIG.    17.      LOW-TENSION   PULSE   TRACING 


FIG.    18.      DICROTIC  PULSE  TRACING 

The  aortic  notch  and  dicrotic  wave  are  well  marked  and  are  situated 
low  on  the  descending  limb,  which  falls  suddenly. 

3.  Virtual-tension  Pulse 

This  variety  of  pulse  is  observed  when  the  element  of  forcible  and 
energetic  heart  beat  is  wanting,  but  the  other  conditions  are  those 
productive  of  high  tension.  These  conditions  obtain  in  the  terminal 
stages  of  Bright's  disease,  when  the  heart  is  failing,  and  in  mitral 
stenosis,  when  the  amount  of  blood  discharged  at  each  systole  into 
the  aorta  is  small. 

Inspection. — If  the  pulse  is  visible  {i.e.  in  the  last  stages  of 
Bright's  disease)  it  rises  and  falls  suddenly.  The  artery  is  large 
and  its  walls  tortuous. 


THE   PULSE  ^7 

Palpation. — The  pulse  may  or  may  not  be  increased  in  frequency. 
It  is  usually  regular  in  force  and  rhythm  until  the  heart  fails  (mitral 
stenosis).  The  vessel  is  usually  large,  but  it  may  be  small,  as  in 
mitral  stenosis. 

The  artery  is  full  between  the  beats  and  fairly  easily  compressible. 
The  wave  rises  rather  suddenly,  is  of  short  duration,  and  falls  some- 
what less  abruptly  than  it  ascends.  The  wave  is  easily  compressed, 
and  the  vessel  wall  is  usually  more  or  less  degenerated. 

Sphygmogram. — The  ascending  limb  is  steep  and  of  considerable 
amplitude,  the  apex  is  acute  and  the  tidal  wave  short.  The  de- 
scending limb  is  somewhat  steep  and  the  dicrotic  wave  is  fairly  well 
marked,  and  is  situated  well  above  the  base  line. 


FIG.    19.      VIRTUAL-TENSION   PULSE   TRACING 

4-   Hypertrophy  of  the  Heart 

The  pulse  in  cases  of  cardiac  hypertrophy  is  that  of  the  condition 
which  has  given  rise  to  the  enlargement  of  the  organ.  Simple 
hypertrophy  of  the  heart  from  prolonged  over-exertion  is  associated 
with  the  following  pulse  : — 

Inspection. — The  arteries  are  often  large,  and  show  regular  and 
forcible  pulsation. 

Palpation. — The  pulse  is  normal  in  frequency  and  regular  in 
force  and  rhythm.  The  vessel  is  often  large,  and  can  usually  be 
felt  between  the  beats.  The  wave  rises  suddenly,  falls  rather 
rapidly,  and  is  fairly  easily  compressible.  The  arterial  wall  is 
healthy. 

Sphygmogram. — Normal,  but  on  rather  a  large  scale. 

5.   Dilatation  of  the  Heart 

As  in  the  case  of  hypertrophy,  dilatation  of  the  heart  is  usually 
associated  with  conditions  which  modify  the  characters  of  the  pulse. 

The  pulse  of  dilatation  of  the  heart  due  to  over-exertion,  or  to 
weakness  of  the  cardiac  walls  following  pyrexia,  the  acute  fevers,  etc., 
needs  a  brief  description. 


88  DISEASES   OF  THE   HEART 

Inspection. — Pulse  not  visible. 

Palpation. — The  frequency  of  the  pulse  is  increased.  The 
pulsations  are  irregular  in  force  and  rhythm.  The  vessel  is  small 
and  cannot  be  felt  between  the  beats.  The  wave  is  small,  and  it 
rises  and  falls  quickly.  The  arterial  wall  may  or  may  not  be 
degenerated. 


PULSE   TRACING    FROM   A   CASE   OF   DILATATION    OF   THE    HEART 
SHOWING   RESPIRATORY  CURVES 


Sphygmograra. — The  tracing  is  very  irregular.  The  dicrotic  wave 
is  usually  present. 

6.  Aortic  regurgitation 

The  collapsing  pulse  of  Corrigan,  or  the  water-hammer  pulse. 

1.  In  valvular  disease 

2.  In  atheroma 

I.    IN   VALVULAR   DISEASE 

Inspection. — The  arteries  of  the  neck,  the  temporal,  subclavian, 
brachial,  and  radial  arteries,  etc.,  show  visible  and  often  violent 
pulsation,  which  exhibits  a  rapid  rise  and  fall.  The  arteries  are 
usually  tortuous  and  more  or  less  thickened  and  degenerated.  The 
tortuosity  is  increased  and  is  associated  with  a  pecuhar  vermiform 
movement  of  the  vessel  as  the  pulse  wave  passes  along  it. 

Palpation. — The  pulse  is  normal  in  frequency  and  regular  in  force 
and  rhythm.  The  vessel  is  large  and  empty  between  the  beats, 
a  feature  that  is  more  readily  appreciated  by  raising  the  wrist  above 
the  level  of  the  shoulder.  The  wave  rises  very  suddenly  and  falls 
with  remarkable  abruptness,  and  is  of  momentary  duration  only. 
It  is  easily  compressible.  The  arterial  wall  is  usually  thickened  and 
may  be  degenerated. 

It  will  be  noted  that  there  is  an  appreciable  delay  in  the  appear- 
ance of  the  pulse  wave  at  the  wrist  after  the  systole  of  the  heart. 
This  loss  of  time  between  the  systole  of  the  ventricle  and  the 
appearance  of  the  pulse  wave  is  peculiar  to  low-tension  pulses,  and 
reaches  its  maximum  development  in  cases  of  aortic  incompetence. 


THE   PULSE 


89 


Capillary  and  venous  pulsation  are  other  phenomena  which  may  be 
seen  in  connection  with  a  relaxed  condition  of  the  arterial  system, 
such  as  obtains  in  cases  of  aortic  regurgitation.  In  these  conditions 
the  relaxed  arterial  walls  fail  to  obliterate  the  pulse  wave,  which 
is  therefore  carried  on  into  the  capillaries  and  thence  into  the  veins. 


FIG.    21.       PULSE   TRACING    FROM    A    CASE   OF   AORTIC    REGURGITATION 

Sphygmogram. — The  ascending  Hmb  is  steep  and  of  great  ampli- 
tude. The  apex  is  very  acute,  and  the  descending  limb  remarkably 
steep.  The  tidal  and  dicrotic  waves  are  hardly  marked  on  the 
tracing,  or  are  altogether  wanting. 

2.  AORTIC   REGURGITATION   DUE   TO   ATHEROMA 
The  regurgitation  in  these  cases  is  due  for  the  most  part  to  dilata- 
tion of  the  root  of  the  aorta  involving  the  aortic  orifice.    The  degree 
of  regurgitation  is  commensurate  with  the  degree  of  dilatation  of  the 
orifice  and  is  usually  slight. 

Inspection. — The  temporal  and  radial  arteries  may  stand  out 
prominently  as  tortuous  cords.  The  pulsation,  when  visible,  will 
appear  to  come  and  go  quickly,  and  may  be  attended  by  loco- 
motion of  the  arteries. 

Palpation. — The  pulse  is  normal  in  frequency  and  regular  in 
force  and  rhythm.  The  artery  is  large  and  full  between  the  beats. 
The  wave  rises  and  falls  suddenly,  and  is  easily  compressible.  The 
wall  of  the  artery  will  show  degenerative  changes.  The  delay  of 
the  pulse  at  the  wrist  is  very  much  less  marked  than  in  aortic 
regurgitation  due  to  valvular  disease. 

Sphygmogram. — The  ascending  limb  is  of  moderate  amplitude 
and  somewhat  steep.  The  descending  limb  is  moderately  steep 
and  shows  an  ill-marked  dicrotic  wave. 


Inspection. - 
Palpation.- 

and  rhythm. 


7.  Aortic  Stenosis 

—The  pulse  is  not  usually  visible. 

-The  pulse  is  normal  in  frequency  and  regular  in  force 
The  artery  is  small  and  can  be  felt  between  the  beats. 


90  DISEASES   OF   THE    HEART 

The  pulse  wave  rises  slowly,  falls  slowly,  and  is  of  considerable 
duration.  It  is  fairly  easily  compressible.  The  condition  of  the 
arterial  wall  is  normal. 


FIG.    22.       PULSE   TRACING    FROM    A    CASE   OF   AORTIC   STENOSIS 

Sphygmogram. — Percussion  wave  absent.  The  tidal  wave  has  an 
ascending  limb  of  low  amplitude,  rising  gradually.  The  apex  is 
rounded  or  flattened.  The  descending  limb  falls  gradually.  The 
dicrotic  wave  is  badly  marked. 

In  cases  of  aortic  stenosis,  and  also  in  other  forms  of  cardio- 
arterial   disease,    tracings   with   a    double    summit   are    sometimes 


FIG.    23.      ANACROTIC   PULSE   TRACING 


FIG.    24.      PULSUS  BISFERIENS 

obtained.  This  is  probably  due  to  an  ineffectual  percussion  wave 
followed  by  a  tidal  wave  of  greater  amplitude.  According  to  Broad- 
bent,  the  double  summit  is  an  example  of  the  pulsus  bisferiens, 
and  is  due  to  a  reinforcement  of  the  ventricular  systole  towards 
its  close. 


THE   PULSE 


91 


8.  Combined  Aortic  Regurgitation  and  Stenosis 

The  pulse  is  the  summation  of  the  effects  produced  by  the  two 
lesions,  with  the  result  that  the  characters  proper  to  each  disease 
are  largely  neutralized. 

Speaking  generally,  the  pulse  will  reflect,  for  the  most  part,  the 
characters  peculiar  to  the  predominating  lesion. 

As  a  rule  the  pulse  is  visible,  regular,  and  more  or  less  collapsing. 

9.  Mitral  Regurgitation 
Inspection. — The  pulse  is  not  usually  visible. 


FIG.    25.      PULSE  TRACING   FROM   A   CASE   OF   MITRAL   REGURGITATION 

Palpation. — The  pulse  is  increased  in  frequency  and  is  irregular 
in  force  and  rhythm.  The  artery  is  small  and  cannot  be  felt  be- 
tween the  beats.  The  wave  rises  and  falls  quickly,  and  is  easily 
compressible.     The  arterial  wall  is  healthy. 

Sphygmogram. — The  tracing  is  often  very  irregular.  The 
ascending  limb  is  of  low  and  irregular  amplitude.  It  rises  rapidly. 
The  apex  is  usually  sharp,  and  the  ascending  limb  falls  quickly. 
The  dicrotic  wave  is  fairly  well  marked,  and  usually  appears  low 
down  on  the  descending  limb. 

10.  Mitral  Stenosis 

Inspection. — The  pulse  is  not  visible. 

Palpation. — The  pulse  is  slightly  increased  in  frequency,  and  is 
regular  in  force  and  rhythm  until  the  heart  fails.  The  artery  is 
small  and  full  between  the  beats.  The  wave  is  small  and  rises  and 
falls  gradually.    It  is  easily  compressed.    The  arterial  wall  is  healthy. 


FIG.    26.       PULSE  TRACING   FROM  A  CASE  OF   MITRAL  STENOSIS 


92  DISEASES   OF   THE   HEART 

Sphygmogram. — The  ascending  limb  rises  gradually  and  is  of 
small  amplitude.  The  apex  is  usually  rounded.  The  descending 
limb  falls  gradually  and  shows  a  badly  marked  aortic  notch  and 
dicrotic  wave. 

In  the  later  stages  of  mitral  stenosis,  with  the  establishment  of 
tricuspid  regurgitation,  etc.,  the  pulse  becomes  very  irregular,  owing 
partly  to  the  fact  that  many  abortive  heart  beats  fail  to  propel  the 
pulse  wave  as  far  as  the  wrist. 

II.  Combined  Mitral  Stenosis  and  Regurgitation 

The  pulse  is  very  irregular  and  small.  It  combines  the  features 
peculiar  to  the  two  lesions,  the  influence  of  the  predominant 
affection  preponderating, 

12.  Combined  Aortic  and  Mitral  Disease 

The  pulse  differs  greatly  in  different  cases.  The  predominating 
lesion  exercises  the  greater  influence  on  the  characters  of  the 
pulse. 

If  aortic  regurgitation  predominates,  the  percussion  wave  is  large 
and  collapse  of  the  pulse  wave  prominent.  If  mitral  regurgitation, 
irregularity  is  the  main  feature.  If  aortic  stenosis,  the  percussion 
wave  is  absent,  the  tidal  wave  taking  its  place.  If  mitral  stenosis, 
the  smallness  of  the  pulse  is  its  most  distinguishing  feature. 

13.  Pulse  of  Aneurism 

The  radial  pulses  on  the  two  sides  may  differ  in  time  and 
character. 

Inspection. — A  visible  pulsation  may  occur  over  the  seat  of  the 
aneurism. 


FIG.    27.       PULSE   TRACING    TAKEN'    FROM    THE    LEFT    RADIAL   ARTERY 
IN   A   CASE   OF   ANEURISM 


Palpation. — The  pulse  is  normal  in  frequency  and  regular  in  force 
and  rhythm.  The  artery  is  small  and  full  between  the  beats.  The 
wave  is  small,  gradual,  prolonged,  and  subsides  gradually.  It  is 
easily  compressible. 


THE    PULSE  93 

Simultaneous  examination  of  the   two  radial   arteries  may  show 
delay  and  altered  character  of  the  pulse  on  the  affected  side. 


FIG.    28.       PULSE   TRACING   TAKEN    FROM    THE    RIGHT    RADIAL   ARTERY 
IN    THE   SAME   CASE    (FIG.    27) 

Sphygmogram. — The  percussion  wave  is  absent.  The  ascending 
limb  of  the  tidal  wave  is  of  low  amplitude  and  rises  slowly.  The 
apex  is  rounded,  and  the  descending  limb  falls  gradually.  The 
dicrotic  and  secondary  waves  are  usually  absent  (Fig.  27). 


THE     INSTRUMENTAL    DETERMINATION     OF 
THE    BLOOD    PRESSURE 

The  digital  estimation  of  the  blood  pressure  obtained  from  a 
peripheral  vessel  like  the  radial  artery  is  liable  to  several  fallacies 
which  may  mislead  even  the  well-trained  finger  (Oliver).  In  order 
to  ensure  accuracy  of  observation,  and  also  to  provide  a  record  for 
the  purposes  of  comparison  and  reference,  it  is  necessary  to  employ 
other  means  of  gauging  the  blood  pressure.  Instruments  which 
fulfil  these  requirements  have  been  devised  by  Hill  and  Barnard 
(the  Sphygmometer);  also  by  Oliver  (the  Hsemodynomometer),  and  by 
others.  The  estimation  of  the  blood  pressure  by  both  instruments 
is  obtained  through  a  fluid  medium,  and  herein  lies  the  accuracy  of 
the  method. 

The  sensitiveness  and  accuracy  of  these  instruments  have  been 
thoroughly  tested,  and  though  the  results  obtained  are  not  beyond 
dispute,  it  is  not  too  much  to  say  that  a  blood  pressure  gauge  should 
form  part  of  the  equipment  of  every  clinician.  Both  the  arterial  and 
venous  blood  pressures  are  capable  of  measurement.  Oliver  states  that 
if  the  influence  of  gravitation  be  excluded  the  arterial  blood  pressure 
is  practically  uniform  throughout  the  arterial  system.  The  average 
mean  arterial  pressure  varies  between  90  and  no  c.mm.  Hg.  It  is 
modified  by  the  age,  weight,  and  build  of  the  individual.  The 
average  venous  pressure  in  recumbency  Oliver  puts  at  10-20  c.mm. 
Hg. 


CHAPTER  V 
THE   CARDIOGRAPH 


Its  Sphere  or  Usefulness — The  Normal  Cardiogram — Cardiograms  of  the  Chief 
Valvular  Lesions. 

The  value  of  the  cardiograph  as  a  means  of  diagnosis  even  in 
skilful  hands  is  somewhat  problematical,  and  in  any  case  the 
results  obtained  are  decidedly  less  trustworthy  than  those  afforded 
by  the  sphygmograph.  The  apex  beat  is  often  difficult  or  im- 
possible to  define,  and  unless  the  button  of  the  instrument  is 
accurately  applied  over  the  site  of  its  manifestation,  the  tracing 
obtained  is  not  that  which  is  due  to  the  actual  impulse  of  the 
heart  against  the  chest  wall,  but  to  movements  in  the  neighbour- 
hood of  the  apex  beat  which  give  the  so-called  "  inverted  tracing." 
If  the  operator  is  not  aware  of  this  possibility  his  results  may  be 
quite  unintelligible. 

Provided,  however,  that  an  accurate  and  reliable  tracing  can  be 


FIG.  29.       NORMAL   CARDIOGRAM 
(Sansom  after  Galabin) 

F  =  Closure  of  semilunar  valves  and  commencement  of  diastole 
K  =  Elevation  due  to  sudden  filling  of  ventricle  by  the  active  dilatation  of  its  walls 
/  =  Period  of  passive  filling  of  ventricle 

a,  =  Auricular  systole  and  completion  of  the  process  of  filling  the  ventricle 
a-d=  Sudden  rise  of  lever  due  to  contraction  of  the  ventricular  wall  at  the  commencement  of 
systole 
d  =  Sudden  opening  of  aortic  valve 
</«'y=  Continued  contraction  of  ventricular  walls 
/=  Closure  of  aortic  valve 

Moie. — «-:/==  systole 
^/i= diastole 

94 


THE   CARDIOGRAPH  95 

obtained,  an  intelligent  interpretation  of  the  cardiogram  may  afford 
diagnostic  evidence  of  some  value.  For  instance,  the  relative 
lengths  of  the  diastolic  and  systolic  periods  of  the  ventricular 
cycle  may  be  gauged  by  this  means  with  some  accuracy.  In 
mitral  stenosis  and  in  dilatation  of  the  left  ventricle  the  diastole  is 
relatively  prolonged,  whereas  in  aortic  regurgitation  and  in  hyper- 
trophy of  the  ventricle  the  same  period  is  relatively  shortened,  and 
hence  the  cardiographic  evidence  in  the  differential  diagnosis  of 
these  affections  may  be  requisitioned  with  advantage. 

In  describing  a  cardiogram  it  is  perhaps  simplest  to  make  use  of 
the  same  nomenclature  as  was  employed  in  the  account  of  the 
sphygmogram. 

Thus  a  cardiogram  may  be  said  to  consist  of  an  ascending  limb 
or  upstroke  {k — d),  an  apex  {ade),  and  a  descending  limb  or  down- 
stroke  {d — ^. 

i/a:  =  diastoHc  rise;  a — ^=  systolic  rise 
d—f=  systolic  fall ;  / — k  =  diastolic  fall 

The  Ascending  Limb 

It  will  be  noticed  that  this  portion  of  the  curve  comprises  both 
diastolic  and  systolic  rises.  The  first  part  of  the  diastolic  rise 
generally  shows  an  elevation  {K)  which  marks  the  filling  of  the 
ventricle  by  its  active  dilatation.  This  elevation  is  particularly  well 
marked  when  the  dilatation  of  the  chamber  is  energetic  as  in  (i) 
hypertrophy  of  the  heart  with  powerful  suction  action  on  dilatation ; 
(2)  low  degrees  of  blood  tension  with  rapid  systole  and  sudden 
relaxation  of  the  ventricle. 

Immediately  following  the  elevation  /^  is  a  gradual  ascent  of  the 
upstroke  /.  It  represents  the  passive  filling  of  the  ventricle 
between  the  first  inrush  of  blood,  due  to  its  active  dilatation,  and 
the  final  act  of  filling  by  the  auricular  systole  a.  The  steepness 
and  length  of  this  part  of  the  curve  depend  largely  on  the  total 
length  of  diastole ;  when  diastole  is  prolonged  this  section  of  the 
curve  is  extensive  and  the  rise  gradual.  When  diastole  is  short  the 
opposite  conditions  obtain.  The  diastolic  rise  sometimes  shows 
elevations  in  addition  to  k  and  a.  These  represent  irregular 
contractions  of  the  auricle,  or  are  due  to  vibrations  of  the  auriculo- 
ventricular  valves. 

The  elevation  a  at  the  end  of  the  diastolic  rise  is  due  to  the 
auricular  systole,  and  is  specially  well  marked  when  the  left  auricle 
is  hypertrophied  as  in  mitral  stenosis. 

As  a  rule  the  elevation  a  is  followed  by  a  notch,  which  separates 
the  diastolic  from  the  systolic  rise.  Sometimes,  however,  this  notch 
is  absent,  in  which  case  the  diastolic  and  systolic  rises  are  continuous. 
The  systolic  rise  varies  in  amplitude  in  different  cases.  Its  height, 
however,  depends  more  on  the  suddenness  of  the  ventricular  systole 
than  on  its  force.     Thus  in  palpitation  and  cases  of  low-tension 


96  DISEASES   OF   THE   HEART 

pulse  the  amplitude  of  this  portion  of  the  tracing  may  be  very 
great,  whereas  in  hypertrophy  the  rise  may  be  comparatively  small. 

The  Apex 

The  degree  of  acuteness  of  this  angle  depends  chiefly  on  the 
suddenness  with  which  the  ventricle  empties  itself,  and  is  due  to  the 
falling  away  of  the  heart's  apex  from  the  chest  wall.  It  is  especially 
acute  in  mitral  regurgitation,  in  which  condition  the  ventricle  has 
two  outlets  by  which  it  can  empty  itself,  viz.  through  the  incom- 
petent mitral  valve  and  through  the  aortic  orifice. 

The  Descending  Limb 

f  marks  the  completion  of  the  systole,  and  the  distance  {d^f), 
i.e.  the  systolic  fall,  is  a  rough  measure  of  the  length  of  the  systole. 
In  hypertrophy  of  the  heart,  and  in  aortic  stenosis,  this  section  of 
the  curve  is  of  considerable  extent,  and  the  apex  is  usually  more  or 
less  rounded. 

f^k,  the  diastolic  fall,  marks  the  beginning  of  diastole  immediately 
after  the  closure  of  the  semilunar  valves.  It  is  usually  nearly  per- 
pendicular, and  occupies,  consequently,  a  very  short  period  before 
the  filling  of  the  ventricle  causes  the  diastolic  rise. 

The  characteristic  features  of  the  cardiograms  taken  from  cases 
representing  the  chief  forms  of  valvular  disease  will  now  be  briefly 
considered. 

MITRAL  STENOSIS 

The  diastolic  rise  is  usually  prolonged,  and  the  elevation  in  it 
due  to  the  auricular  systole  is  well  marked.  There  may  be  secondary 
elevation  on  this  limb  of  the  cardiogram,  due  to  the  causes  enumer- 
ated above. 


FIG.   30.       CARDIOGRAM   FROM   A    CASE   OF    MITRAL   STENOSIS 
(Sansom) 

In  this  tracing  the  diastohc  rise  is  of  considerable  length  and 
inclined  obliquely  upwards,  showing  the  long  period  occupied  in 


THE   CARDIOGRAPH 


97 


the  filling  of  the  ventricle  through  the  narrowed  mitral  orifice. 
Secondary  undulations  are  present  on  this  section  of  the  tracing, 
due  to  irregular  contractions  of  the  auricle,  or  to  vibrations  set  up 
at  the  mitral  valve.  The  elevation  due  to  the  auricular  systole  is 
not  sufficiently  well  marked  to  suggest  great  hypertrophy  of  the  left 
auricle. 


FIG.  31. 


CARDIOGRAM    FROM   A   CASE   OF   MITRAL  STENOSIS 
(Sansora) 


This  tracing  shows  great  irregularity  of  the  heart's  action,  which 
is  due  to  the  supervention  of  heart  failure  with  tricuspid  regurgitation. 


FIG.  32.       CARDIOGRAM    FROM    A    CASE   OF    MITRAL   STENOSIS 
(Sansom  after  Galabin) 

This  tracing  shows  a  great  elongation  of  the  "diastolic  rise" 
section  of  the  ascending  limb. 

MITRAL  REGURGITATION 


FIG.  33. 


CARDIOGRAM    FROM   A   CASE  OF   MITRAL   REGURGITATION 

(Sansom) 


This  cardiogram  shows  great  irregularity  of  the  heart's  action. 
The  length  of  the  diastolic  rise  is  very  variable,  and  the  rise  due 
to  the  auricular  systole  is  badly  marked.     The  apex  is   bifid,  the 

H 


98  DISEASES   OF   THE    HEART 

second   elevation    being   due   to   the   contraction   of    the   musculi 
papillares  (Roy  and  Adami). 

AORTIC   STENOSIS 


FIG.  34.      CARDIOGRAM   FROM   A  CASE  OF  AORTIC  OBSTRUCTION 
(Sansom  after  Galabin) 

Owing  to  the  prolonged  ventricular  contraction  the  systolic  rise 
is  gradual  and  the  apex  rounded.  The  total  systolic  period  is 
lengthened,  and  the  diastolic  rise  short. 

AORTIC   REGURGITATION 


FIG.  35.      CARDIOGRAM  AND   SPHYGMOGRAM   FROM   A  CASE   OF 

AORTIC   REGURGITATION 

(Sansom) 

The  diastolic  rise  is  steep,  owing  to  the  rapid  filling  of  the 
ventricles  due  to  the  regurgitation.  The  systolic  rise  is  steep,  owing 
to  the  sudden  contraction  of  the  ventricle.  The  apex  is  acute^  and 
the  systolic  fall  steep. 


CHAPTER  VI 

CONGENITAL   AFFECTIONS    OF   THE 
HEART  AND  GREAT  VESSELS 


Etiology  and  Pathology — Classification — Symptoms — Physical  Signs — Diagnosis 
— Prognosis — Treatment. 

iETIOLOGY    AND    PATHOLOGY 

Malformations  and  misplacements  of  the  heart  represent,  for  the 
most  part,  permanent  survivals  of  foetal  conditions.  A  short  ac- 
count, therefore,  of  the  development  of  the  cardio-vascular  system, 
in  so  far  as  it  bears  on  this  subject,  will  render  the  mode  of  origin 
of  the  congenital  affections  of  the  heart  and  great  vessels  more 
intelligible  to  the  reader. 

At  an  early  period  of  development  the  heart  consists  of  two  sepa- 
rate tubes  of  mesoblast,  which  coalesce  in  the  median  line  soon 
after  the  thirteenth  day,  to  form  in  the  upper  part  of  the  neck  a 
tube  of  single  bore,. which  is  slightly  twisted  on  itself.  As  develop- 
ment proceeds  this  tube  loses  all  traces  of  its  original  double  bore, 
and  during  the  third  week  a  constriction  appears  which  marks  the 
primitive  division  into  auricle  and  ventricle,  the  former  lying  some- 
what behind  {i.e.  posterior)  to  the  latter.  At  the  same  time  the  tube 
becomes  further  removed  from  the  cephalic  end  of  the  foetus,  and 
gravitates  as  a  whole  towards  the  position  it  finally  occupies  in  the 
thorax. 

The  tube  then  becomes  twisted  upon  itself  in  such  a  way  that  the 
auricular  portion  comes  to  lie  behind  and  below  the  ventricular 
portion.  The  single  auricle  receives  the  two  vente  cavse,  and  the 
single  ventricle  gives  rise  to  the  common  arterial  trunk  [truncus 
arteriosus). 

The  constriction  between  the  primarily  undivided  auricle  and 
ventricle  appears  internally  as  a  ridge  of  tissue  (the  primitive 
auriculo-ventricular  septum),  which,  by  means  of  two  localized  out- 
growths (the  endocardial  cushions)  from  points  on  opposite  sides  of 
the  tube,  effects  a  median  junction,  with  the  result  that  two  passages 
are  formed — the  right  and  left  auriculo-ventricular  openings. 

99 


lOO  DISEASES   OF   THE    HEART 

The  auricle  undergoes  division  before  the  ventricle. 

The  septum  first  appears  at  the  upper  and  posterior  part  of  the 
auricular  cavity,  and  the  free  edge  grows  forwards  and  downwards  to 
join  with  the  fused  cushion-like  thickenings  which  divide  the  auriculo- 
ventricular  orifices,  and  also  form  part  of  the  interventricular  septum. 

Before  the  completion  of  the  auricular  septum  a  new  orifice,  the 
foramen  ovale,  makes  its  appearance  at  the  upper  and  posterior  part 
of  this  structure.  The  closure  of  the  foramen  ovale  is  effected  at  a 
later  period  by  the  development  of  a  second  septum,  which  also 
grows  from  the  superior  auricular  wall,  a  little  to  the  right  of  the 
original  partition.  The  new  septum  grows  forward,  and  acts  as 
a  valve  or  curtain,  which  is  gradually  drawn  over  the  foramen  ovale, 
and  at  birth  completely  closes  the  opening. 

The  septum  atriorum  is  situated  to  the  left  of  the  orifices  of  the 
superior  and  inferior  venae  cavse,  and  hence  these  vessels  discharge 
their  contents  into  the  right  auricle.  The  pulmonary  veins  are,  at 
an  early  date,  found  in  connection  with  the  left  auricle. 

The  ventricle  subsequently  undergoes  division  into  two  cavities  by 
the  evolution  of  the  interventricular  septum,  which  has  a  triple 
origin,  namely,  from  (i)  a  muscular  upgrowth  from  the  antero- 
inferior part  of  the  primitive  ventricle ;  (2)  the  endocardial  cushions, 
which  divide  the  common  auriculo-ventricular  orifice  into  a  right  and 
left  half;  and  (3)  the  septum,  which  divides  the  common  arterial 
trunk  into  an  aortic  and  pulmonic  moiety.  The  interventricular 
septum  is  completed  by  the  fusion  of  these  three  segments.  It 
is  the  anterior  part  of  the  septum,  viz.  the  portion  which  lies 
between  the  two  arterial  orifices,  which  is  most  commonly  the  seat 
of  incomplete  development.  Less  frequently  the  posterior  segment, 
which  is  situated  between  the  two  auriculo-ventricular  openings,  is 
partially  or  entirely  absent. 

The  membranous  portion  of  the  septum  is  the  part  which  lies 
between  the  anterior  and  posterior  sections.  It  has  been  called  the 
undefended  space  by  English  authors. 

This  membranous  portion  has  been  regarded  as  the  part  of  the 
septum  which  is  most  liable  to  defects  of  development.  Roki- 
tansky  has,  however,  conclusively  shown  that  of  all  sections  of  this 
structure  it  is  the  least  liable  to  malformation. 

DEVELOPMENT  OF  THE  GREAT  VESSELS  IN  RELATION 
WITH  THE  HEART 

The  two  primitive  tubes  which  coalesce  and  constitute  the  heart 
continue  fused  together  for  a  short  distance  beyond  this  viscus,  and 
form  the  common  arterial  trunk  or  conus  arteriosus. 

At  a  later  period  this  vessel  becomes  differentiated  into  the  aorta 
and  pulmonary  artery  by  the  development  of  a  longitudinal  septum, 
which  divides  the  originally  single  tube  into  two  portions.  This 
septum  ultimately  effects  a  junction  below  with  the  interventricular 


CONGENITAL  AFFECTIONS  OF  THE  HEART     loi 

and  interauricular  septa  in  such  a  way  that  it  not  only  completes  the 
separation  of  the  ventricles,  but  also  cuts  the  connection  between 
the  aorta  and  right  ventricle,  and  places  this  vessel  exclusively  in 


Left 
Subclanan 


Obliterated  5'!^  arch 


Dorsal  Jiortcu 


FIG.  36.      THE  AORTIC  ARCHES,  SHOWING  MODE  OF  TRANSFORMATION  INTO 

PERMANENT  ARTERIAL  TRUNKS.      THE  PARTS  IN  BLACK  BECOME  OBLITERATED 

(After  MacAlister,  modified) 


communication  with  the  left  ventricle.  Above,  the  disposition  of 
the  septum  is  such  that  it  directs  blood  coming  from  the  right 
ventricle  into  the  ductus  arteriosus,  or  fifth  arch,  leaving  a  small 
communication    only   between   the    aorta   and    pulmonary   artery. 


102  DISEASES   OF  THE    HEART 

Finally  this  opening  is  also  closed,  so  that  at  birth  the  right  ventricle 
pours  the  whole  of  its  contents  into  the  pulmonary  artery,  whereby 
its  area  of  distribution  is  confined  to  the  lungs. 

The  two  primitive  tubes  beyond  the  conus  arteriosus  continue  as 
separate  structures  towards  the  cephalic  end  of  the  foetus,  and  on 
each  side  supply  in  succession  branches  which  ascend  between  the 
visceral  clefts,  and  unite  again  at  the  posterior  extremity  of  these 
clefts  to  form  a  single  vessel  on  each  side.  These  two  vessels,  the 
primitive  descending  aortse,  run  down  the  trunk  on  either  side  of 
the  notochord,  giving  off  as  they  descend  lateral  branches  to  the 
body  wall  and  yolk  sac,  and  terminate  in  two  large  vessels  which 
accompany  the  allantois,  and  furnish  blood  to  the  foetal  portions  of 
the  placenta. 

The  two  primitive  descending  aortge  at  an  early  period  of  develop- 
ment coalesce  immediately  behind  {i.e.  posterior  to)  the  heart  to 
form  a  single  tube,  which  runs  in  the"'  median  line  up  to  its 
bifurcation  into  the  two  common  iliac  arteries.  Above  their  point 
of  junction  the  two  primitive  vessels  remain  as  single  tubes  on 
either  side  of  the  notochord.  The  tube  on  the  right  side  ultimately 
disappears,  while  the  one  on  the  left  persists  as  the  first  part  of  the 
descending  aorta,  and  becomes  directly  continuous  below  with  the 
single  fused  vessel  (Fig.  36). 

The  branches  or  arches,  as  they  are  called,  which  arise  on  either 
side  from  the  two  primitive  vessels  forming  the  continuation  of  the 
truncus  arteriosus  and  pass  between  the  visceral  clefts,  are  five  in 
number.  The  first  three  are  not  of  any  interest,  so  far  as  the 
subject  under  discussion  is  concerned.  The  destinations  of  the 
fourth  and  fifth  arches  are,  however,  of  great  importance,  as  they 
bear  directly  on  the  question  of  cardiac  malformations. 

The  fourth  arch  on  the  right  side  forms  the  arteria  innominata  and 
root  of  the  right  subclavian  artery.  On  the  left  side  it  persists  as 
the  aortic  arch  and  first  part  of  the  descending  aorta.  The  fifth 
arch  on  the  right  side  becomes  obliterated.  The  fifth  left  arch,  or 
ductus  arteriosus,  persists  throughout  its  entire  length  during  intra- 
uterine life.  It  joins  the  continuation  of  the  fourth  arch  on  the 
left  side,  and  is  therefore  continuous  with  the  descending  aorta  and 
umbilical  arteries.  Moreover,  since  the  ductus  arteriosus,  through 
the  pulmonary  artery,  is  in  direct  continuity  with  the  right  ventricle, 
the  foetal  portions  of  the  placenta  are  chiefly  supplied  with  blood 
from  the  right  heart.  At  birth,  with  the  expansion  of  the  lungs,  the 
distal  connection  of  the  ductus  arteriosus  with  the  aorta  becomes 
obliterated,  and  forms  a  fibrous  cord,  the  ligamentum  arteriosum. 

The  proximal  end  of  the  ductus  arteriosus,  however,  persists  as 
the  pulmonary  artery. 

In  the  light  of  the  developmental  connections  of  the  great 
vessels,  it  is  obvious  that  in  cases  of  pulmonic  stenosis,  or  in  con- 
ditions affecting  the  patency  of  the  pulmonary  artery  during  foetal 
life,  the  blood  supply  to  the  lungs  after  birth  can  be  supplemented 


CONGENITAL  AFFECTIONS  OF  THE  HEART     103 


FIG.  37.      DIAGRAMMATIC   OUTLINE   OF   THE  ORGANS   OF   CIRCULATION 

IN   THE  FCETUS   OF  SIX  MONTHS 

(Thompson,  Quain's  Anatomy) 

RA=right  auricle;  RV  =  right  ventricle;  LA = left  auricle  ;  Ev = eustachian  valve ;  LV= 
left  ventricle;  L  =  liver;  K  =  left  kidney;  I  =  portion  of  small  intestine;  a!=arch  of  aorta; 
«'  =  its  dorsal  part;  a"  =  its  lower  end;  z'i'^  =  superior  vena  cava;  z/cz  =  inferior  vena  cava 
where  it  joins  the  right  auricle  ;  vcV  =  '\\.%  lower  end  ;  ^=subclavian  vessels  ;  y=right  jugular 
vein;  c=common  carotid  arteries;  four  curved  dotted  arrow  lines  are  carried  through  the 
aortic  and  pulmonary  opening  and  the  auriculo-ventricular  orifices ;  da,  opposite  to  the  one 
passing  through  the  pulmonary  artery,  marks  the  place  of  the  ductus  arteriosus  ;  a  similar 
arrow  line  is  shown  from  the  vena  cava  inferior  through  the  fossa  ovalis  of  the  right  auricle 
and  the  foramen  ovale  into  the  left  auricle. 


104  DISEASES   OF   THE    HEART 

by  way  of  the  aorta  through  either  extremity  of  the  ductus 
arteriosus. 

Conversely,  the  blood  current  through  the  aorta,  in  case  of 
obstruction  at  the  aortic  orifice  or  in  the  course  of  the  vessel, 
can  be  reinforced  by  way  of  the  pulmonary  artery  or  its  continua- 
tion, the  ductus  arteriosus  (Fig.  37). 

In  want  of  a  more  scientific  explanation,  the  malformations  of  the 
heart  and  great  vessels  are  commonly  ascribed  to  congenital  errors 
of  development,  or  to  hereditary  deficiency  of  developmental 
power.  Expressions  of  this  kind  avoid  physical  explanations,  and 
are  little  more  than  admissions  of  our  ignorance  of  the  true  causes 
of  congenital  cardiac  anomalies.  It  is  probable,  however,  that 
when  more  than  one  member  of  the  same  family  has  been  the 
subject  of  a  similar  cardiac  malformation  there  has  been  the  same 
mechanical  cause  at  work,  although  it  is  not  possible,  in  the  present 
state  of  our  knowledge,  to  demonstrate  its  nature. 

Maternal  impressions  have  also  been  held  responsible  for  a  con- 
siderable number  of  cardiac  malformations,  a  belief  which  is  founded 
more  on  popular  superstition  than  on  scientific  reasoning. 

On  the  other  hand,  there  are  a  considerable  number  of  cases 
of  cardiac  mal-development  for  which  we  can  assign  approximate 
physical  causes,  although  it  may  be  that  in  some  of  these  instances 
a  link  here  and  there  in  the  chain  of  argument  is  forged  on  a 
theoretical  hypothesis. 

After  birth,  the  strain  which  may  be  imposed  on  the  aortic  and 
mitral  valves  by  increased  arterio  -  capillary  resistance,  and  the 
variable  demands  made  upon  the  left  side  of  the  heart  by  altera- 
tions in  blood  pressure,  not  only  predispose  to  valvular  inflammation, 
but  also  frequently  induce  structural  changes  in  the  cavity  and  wall 
of  the  left  ventricle.  If  organic  changes  of  this  character  can  be 
wrought  in  the  completely  developed  heart,  it  is  hardly  surprising 
that  similar  conditions  operating,  in  utero,  on  a  heart  which  is  in 
process  of  evolution  should  evoke  alterations  as  profound  and 
extensive  as  those  in  clinical  records. 

The  foetus,  as  it  lies  in  utero,  is  to  a  large  extent  protected  from 
disturbances  of  blood  pressure,  so  far  as  its  intrinsic  circulation  is 
concerned.  Nevertheless,  the  circulation  through  the  umbilical 
cord,  as  well  as  through  the  foetal  portion  of  the  placenta,  must, 
in  the  ordinary  course  of  events,  be  exposed  to  considerable 
variations  in  blood  pressure.  It  has  already  been  shown  that  the 
umbilical  arteries  are  branches  of  the  descending  aorta,  which  for 
the  most  part  receives  its  blood  supply,  through  the  ductus  arteriosus, 
from  the  right  ventricle.  Hence,  in  the  foetus  it  is  the  right  side  of 
the  heart,  with  its  included  valvular  mechanisms,  which  bears  the 
brunt  of  the  circulation.  Consequently  we  should  expect  that  a 
departure  from  the  normal  course  of  development  would  be  more 
liable  to  occur  on  the  right  than  on  the  left  side  of  the  heart. 
Statistics  bear  out  this  reasoning,  for  out  of  181  cases  of  cardiac 


CONGENITAL  AFFECTIONS  OF  THE  HEART     105 

malformation  collected  by  Peacock  119  were  associated  with  lesions 
at  the  pulmonic  orifice. 

Furthermore,  if  it  be  admitted  that  defects  of  development  may 
be  produced  at  the  pulmonic  orifice  by  mechanical  causes  in  the 
manner  that  has  been  suggested,  it  is  comparatively  easy  to  assign 
a  physical  reason  for  other  and  secondary  structural  imperfections 
which  may  be  found  in  association  with  these  lesions. 

The  abnormalities  of  development  to  which  attention  will  be 
especially  directed  are  those  affecting  (i)  the  interventricular  septum, 
(2)  the  interauricular  septum,  (3)  the  junction  of  the  aorta  with  the 
right  or  left  ventricle,  (4)  the  patency  of  the  ductus  arteriosus. 

If  the  pulmonary  artery  or  its  orifice  become  the  seat  of  obstruc- 
tion, so  that  the  passage  of  blood  through  the  vessel  is  interfered 
with,  before  the  division  of  the  ventricles  is  completed  by  the  junc- 
tion of  the  septum  of  the  conus  arteriosus  with  that  of  the  ventricles, 
the  increase  of  pressure  in  the  right  ventricle,  by  causing  a  flow  of 
blood  from  one  side  of  the  heart  to  the  other  during  systole,  may 
delay  or  altogether  prevent  the  union  of  these  two  segments  of  the 
interventricular  partition.  Under  these  circumstances  the  aorta  may 
not  only  communicate  with  the  left,  but  also  with  the  right  ventricle 
through  the  deficiency  in  the  septum.  Moreover,  this  condition  may 
become  a  permanent  one,  so  that  as  long  as  life  is  maintained  both 
the  aorta  and  pulmonary  artery  are  conjointly  fed  by  the  right  and 
left  ventricles. 

The  septum  of  the  ventricles  may,  however,  be  partially  incom- 
plete, although  the  septum  of  the  conus  arteriosus  has  fused  with 
that  of  the  ventricles,  and  thus  established  direct  communication 
between  the  aorta  and  left  ventricle  and  between  the  pulmonary 
artery  and  right  ventricle.  In  such  an  event,  if  stenosis  of  the 
pulmonic  orifice  occur,  the  blood  (owing  to  the  rise  of  pressure  in 
the  right  ventricle  consequent  on  the  difificulty  in  the  discharge  of 
its  contents)  takes  the  path  of  least  resistance  through  the  opening 
in  the  septum  into  the  left  ventricle.  The  constant  irritation  and 
disturbance  thus  produced  will  delay  or  prevent  the  completion  of 
the  interventricular  septum. 

Again,  the  obstruction  to  the  passage  of  blood  through  the  pul- 
monic orifice  may  arise  after  the  completion  of  the  interventricular 
septum,  but  while  there  is  still  a  communication  between  the  two 
auricles  through  the  foramen  ovale.  In  this  event  the  increase  of 
pressure  in  the  right  ventricle  gives  rise  to  more  or  less  regurgi- 
tation into  the  right  auricle,  so  that  part,  at  least,  of  the  blood 
current  is  diverted  into  the  left  auricle  through  the  patent  foramen 
ovale. 

If  the  degree  of  pulmonic  stenosis  is  moderate,  the  right  ventricle 
hypertrophies,  owing  to  the  difficulty  experienced  in  the  discharge  of 
its  contents  ;  the  left  ventricle  hypertrophies  from  overwork,  and  the 
ductus  arteriosus  may  or  may  not  remain  patent  after  birth. 

If  the  degree  of  pulmonic  stenosis  is  very  great,  the  right  ventricle 


io6  DISEASES   OF   THE    HEART 

ultimately  atrophies,  and  is  practically  thrown  out  of  the  circulation  ; 
the  left  ventricle  hypertrophies  from  overwork,  and  after  birth  supplies 
the  lungs  with  blood  through  the  aorta  and  patent  ductus  arteriosus. 

In  like  manner,  obstruction  on  the  left  side  of  the  heart  deter- 
mines corresponding  anomalies  of  development. 

Stenosis  of  the  aortic  opening  may  divert  the  blood  flow  through 
the  imperfect  septum  of  the  auricles  or  ventricles  into  the  right  side 
of  the  heart,  and  thus,  by  constant  irritation,  prevent  the  perfect 
evolution  of  these  structures.  The  right  side  of  the  heart  then 
carries  on  both  the  systemic  and  pulmonic  circulations,  the  pul- 
monary artery  dividing  its  contents  between  the  ductus  arteriosus 
and  aorta  above  the  seat  of  obstruction. 

Deficiency  of  the  interauricular  or  interventricular  septum  is  not 
only  compatible  with  life,  but  also  with  a  healthy,  well-organized  life, 
so  soon  as  the  heart  becomes  balanced  to  the  altered  conditions  of 
the  circulation. 

It  has  been  shown,  therefore,  how  obstruction  at  one  or  other  of 
the  orifices  of  the  heart  may  determine  the  further  course  of  develop- 
ment. In  the  instances  which  have  been  given,  the  obstruction  has 
occurred  at  a  somewhat  late  period  in  the  evolution  of  the  organ. 
There  is  no  reason  why  interference  with  the  circulation  through  the 
heart  and  great  vessels  should  not  occur  at  earlier  periods,  and 
exercise  an  influence  similar  in  kind  but  more  far-reaching  in  its 
effects,  and  thus  determine  errors  in  development  for  which  we  can 
otherwise  find  no  satisfactory  explanation. 

In  the  attempt  which  has  been  made  to  show  that  abnormalities 
in  the  development  of  the  heart  depend  in  a  large  measure  on 
mechanical  causes,  no  mention  has  been  made  of  demonstrable 
inflammatory  conditions  of  the  valves  and  endocardium.  Endo- 
carditis does,  however,  occasionally  occur  in  intra-uterine  life,  and 
gives  rise,  for  the  most  part,  to  stenosis  of  the  orifice,  which  is  the 
seat  of  the  inflammatory  process.  The  effects  of  the  lesion  on  the 
further  course  of  the  development  of  the  heart  are  similar  in  kind 
to  those  produced  by  stenosis  of  the  orifices  from  other  causes. 

The  form  of  endocarditis  most  commonly  observed  is  the  chronic 
or  sclerotic  variety.  It  usually  occurs  on  the  right  side  of  the  heart, 
for  two  reasons  :  firstly  because  the  right  side  of  the  heart  is  exposed 
to  greater  strain  than  the  left,  and  secondly  because  malformations 
occur  more  commonly  on  the  right  side  of  the  organ,  and  inflamma- 
tory conditions  appear  to  become  more  readily  superimposed  on 
imperfectly,  than  on  perfectly  developed  structures. 

The  exciting  causes  of  foetal  endocarditis  are  probably  blood  con- 
ditions existing  in  the  mother,  which  are  transmitted  to  the  embryo 
through  the  foetal  circulation. 

CLASSIFICATION 

Congenital  affections  of  the  heart  occur  either  as  misplacements 
or  malformations  of  the  organ. 


CONGENITAL  AFFECTIONS  OF  THE  HEART     107 

MISPLACEMENTS   OF  THE   HEART 

I.  Dextro-cardia  is  the  condition  in  which  the  heart  occupies 
a  position  in  the  chest  which  may  be  described  as  the  "  negative  " 
of  its  ordinary  position. 

In  its  relation  to  the  middle  line  the  heart  normally  lies  obliquely 
with  its  apex  pointed  to  the  left.  In  the  condition  under  discussion 
the  organ  points  to  the  right.  The  heart  should  lie  not  presenting 
its  two  sides  in  equal  degree  to  the  front,  but  turned  on  its  axis, 
so  that  the  right  ventricle  looks  forwards,  and  the  left  backwards. 
In  the  condition  of  dextro-cardia,  the  left  ventricle  looks  forwards 
and  the  right  ventricle  backwards.  The  heart  should  not  lie  in 
the  middle  vertical  line  of  the  body,  but  should  be  placed  somewhat 
tilted  forwards,  so  that  its  apex  lies  in  advance  of  its  base.  In  the 
abnormal  condition  this  relation  is  still  maintained. 

The  original  position  of  the  heart  in  the  embryo  is  in  the  course 
of  development  normally  altered  by  twists  in  three  directions. 

From  the  vertical  middle  line  it  is  twisted  to  the  left;  on  its 
vertical  axis  it  is  twisted  to  the  left ;  on  the  horizontal  Hne  it  is 
twisted  to  the  front.  In  the  abnormal  condition  under  discussion 
the  two  first-mentioned  twists  are  reversed,  while  the  third  remains 
as  in  the  normal  state. 

Clinically,  the  result  of  this  abnormality  is  that  the  apex  of  the 
heart  is  found  on  the  right  instead  of  the  left  side  of  the  chest, 
and  the  bulk  of  the  organ  is  situated  to  the  right  instead  of  to  the 
left  of  the  median  line.  Nothing  more  can  be  discovered  at  the 
bedside,  but,  post-mortem  the  aorta  and  pulmonary  artery  are  also 
reversed  in  their  directions. 

Dextro-cardia  may  be  found  as  an  independent  condition,  but 
it  is  usually  associated  with  transposition  of  the  other  viscera.  Thus 
the  liver  is  on  the  left  side,  the  stomach  and  spleen  on  the  right. 
The  caecum  is  on  the  left,  the  sigmoid  flexure  on  the  right,  while 
the  left  lung  has  three  lobes,  and  the  right  two  only.  No  symptoms 
whatever  result  from  this  condition,  but  its  clinical  importance 
arises  from  the  liability  to  mistake  the  misplacement  of  the  heart 
and  viscera  for  other  conditions,  the  outcome  of  disease. 

2.  Mesocardia. — In  this  condition  the  heart  occupies  a  central 
position  in  the  thorax,  a  situation  normal  to  it  in  the  early  stages 
of  development. 

3.  Ectopia  cordis. — This  abnormality  occurs  in  three  forms — 

1.  Ectopia  cervicalis 

2.  Ectopia  pectoralis 

3.  Ectopia  abdominali-i 

I.  Ectopia  cervicalis  is  an  extreme  case  of  misplacement,  in  which 
the  heart  occupies  a  position  in  close  proximity  to  the  lower  jaw. 
The  organ  may  be  exposed  or  covered  with  a  layer  of  skin. 


io8  DISEASES   OF   THE   HEART 

2.  Ectopia  pedoralis  is  usually  associated  with  more  or  less  de- 
ficiency of  the  sternum  and  thoracic  wall.  The  heart  may  be  freely 
exposed,  or  covered  by  its  pericardium  only,  or  by  skin  and  peri- 
cardium. 

T,,  Ectopia  abdominalis  is  the  form  in  which  the  heart  lies,  below  the 
diaphragm,  in  the  abdominal  cavity. 

The  two  first-mentioned  varieties  of  ectopia  cordis  are  hardly 
compatible  with  extra-uterine  life.  In  the  third  variety  life  has  been 
maintained  for  some  years. 

MALFORMATIONS  OF  THE  HEART 

Deficiency  of  the  pericardium. — Complete  absence  of  the  peri- 
cardium is  exceedingly  rare  as  an  independent  condition. 

In  most  instances  complete  absence  of  the  pericardium  is  found  in 
association  with  ectopia  cordis.    Partial  defect  is  sometimes  observed. 

Abnormalities  of  the  cardiac  wall. — Hypertrophy  or  atrophy  of 
one  or  other  of  the  chambers  of  the  heart  is  not  uncommonly 
found.  The  only  other  abnormality  in  this  class  that  requires  notice 
is  the  condition  known  as  divided  or  bifid  apex,  which  has  no 
clinical  interest. 

Anomalies  of  the  cardiac  septa. — In  very  rare  instances  both  the 
interauricular  and  interventricular  septa  are  entirely  absent.  The 
heart  then  consists  of  two  cavities,  and  the  condition  is  termed 
"cor  biloculare." 

In  still  rarer  cases  the  interauricular  septum  persists  while  the 
interventricular  septum  is  completely  absent,  so  that  the  heart 
consists  of  three  cavities,  the  so-called  "cor  triloculare." 

Complete  absence  of  the  interauricular  septum  with  persistence  of 
the  interventricular  septum  is  extremely  rare. 

Interventricular  septum. — Partial  deficiency  of  this  septum  is 
not  uncommon.  The  deficiency  usually  affects  the  hinder  part  of 
the  anterior  section  just  in  front  of  the  membranous  portion  of  the 
partition.  Less  commonly  the  posterior  part  of  the  septum  is  de- 
ficient.   In  rare  instances  the  membranous  portion  is  found  wanting. 

Interauricular  septum. — Partial  defects  of  this  septum  are  not  in- 
frequently observed.     The  abnormalities  which  may  be  found  are — 

1.  Absence  of  the  anterior  muscular  portion  of  the  septum. 

2.  Complete  patency  of  the  foramen  ovale. 

3.  Incomplete  closure  of  the  foramen  by  the  valve. 

4.  Perforations  round  the  edge  of  the  membrane  which  closes  the 

foramen. 

5.  An  oblique  opening  beneath  the  edge  of  the  valve  when  this 

membrane  is  not  united  to  the  anulus. 

6.  The  membrane  which  should  close  the  foramen  may  be  more 

or  less  cribriform  in  structure. 


CONGENITAL  AFFECTIONS  OF  THE  HEART     109 
ANOMALIES  OF  THE  VALVES  OF  THE  HEART 

The  Semilunar  Valves 

These  valves  may  consist  of  two  cusps  only,  or  by  the  develop- 
ment of  supernumerary  segments  their  number  may  be  increased 
to  four  or  five. 

The  pulmonic  orifice  and  artery. — The  following  forms  of  ob 
struetion  at  this  orifice,  and  in  the  course  of  the  vessel,  are  found : — 

1.  Stenosis  of  the  pulmonic  orifice  frequently  found  in  association 

with  defects  of  the  cardiac  septa. 

2.  Atresia  of  the  orifice  and  first  part  of  the  pulmonary  artery. 

3.  Stenosis  of  the  trunk  and  canal  of  the  pulmonary  artery. 

4.  Stenosis  of  the  conus  arteriosus.    In  this  event  the  infundibular 

portion  of  the  right  ventricle  is  the  part  chiefly  affected. 

The  aortic  orifice  and  aorta. — The  following  abnormalities  are 
observed  : — 

1.  Stenosis  of  the  aortic  orifice. 

2.  Atresia  of  the  orifice  and  first  portion  of  the  aorta. 

3.  Stenosis  of  the  arch  of  the  aorta  at  the  ductus  arteriosus.    This 

is  a  very  rare  condition,  and  is  due  to  a  too  great  extension 
of  the  cicatricial  process  involved  in  the  closure  of  the 
ductus  arteriosus. 

The  Auriculo- Ventricular  Valves 

The  mitral  valve  may  consist  of  three  flaps.  The  edges  of  the 
curtains  of  the  valve  may  be  united  to  form  a  continuous  membrane 
with  a  central  aperture. 

The  tricuspid  valve  may  consist  of  four  or  more  flaps.  The 
edges  of  the  curtains  may  be  adherent  with  the  production  of 
stenosis  of  the  orifice. 

Anomalies  of  the  tricuspid  valve  frequently  coexist  with  defects 
of  development  at  the  pulmonic  orifice. 

ANOMALIES   OF   THE   LARGE  VESSELS 

1.  Transposition  of  the  aorta  and  pulmonary  artery,  either  with 

or  without  transposition  of  the  mitral  and  tricuspid  valves,  is 
sometimes  observed. 

2.  The  septum  between  the  aorta  and  pulmonary  artery  may  be 

wholly  or  partially  deficient,  so  that  the  two  vessels  com- 
municate with  each  other. 


no  DISEASES   OF    THE    HEART 

3.  Persistence  of  the  ductus  arteriosus. 

The  closure  of  this  vessel  usually  takes  place  within  a  few 
days  after  birth.  If  the  normal  process  of  involution  fails,  a 
communication  is  left  between  the  aorta  and  the  left  branch 
of  the  pulmonary  artery.  The  result  is  more  or  less  regurgi- 
tation from  the  aorta  into  the  lungs.  Patency  of  the  ductus 
arteriosus  is  usually  associated  with  other  developmental 
anomalies  of  the  heart. 

4.  Premature  closure  of  the  ductus  arteriosus. 

This  condition  is  usually  associated  with  imperfect  de- 
velopment of  the  pulmonary  artery. 

Pathologically  the  most  common  congenital  anomalies  of  the  heart 
are  stenosis  of  the  pulmonary  artery,  defects  of  the  cardiac  septa, 
and  abnormalities  of  the  sigmoid  valves. 

SYMPTOMS 

The  symptoms  which  arise  in  connection  with  congenital  affections 
of  the  heart  are  referable,  for  the  most  part,  to  derangements  of  the 
circulation. 

The  earliest  and  most  characteristic  feature  of  congenital  disease 
of  the  heart  is  cyanosis.  It  occurs  in  about  90  per  cent,  of  the  cases, 
and  the  degree  of  its  manifestation  varies  between  a  slight  lividity 
and  a  dark  purple  discoloration  (see  p.  23).  The  extremities,  the 
ears,  nose,  and  face  are  the  parts  through  which  the  circulation  is 
maintained  with  the  least  facility,  and  consequently  it  is  in  these 
situations  that  the  cyanosis  is  most  marked. 

If  the  cardiac  lesion  is  compatible  with  life,  the  further  develop- 
ment and  nutrition  of  the  tissues  in  general,  and  of  the  above- 
mentioned  parts  in  particular,  are  seriously  interfered  with.  Growth 
is  stunted,  the  fingers  and  toes  become  club-shaped,  often  in  associa- 
tion with  a  claw-like  appearance  of  the  nails,  and  unhealthy  sores 
may  arise  in  various  parts  of  the  body. 

It  is  somewhat  anomalous  that  dropsy  is  seldom  observed  with 
congenital  affections  of  the  heart,  although  the  conditions  which  are 
apparently  essential  for  its  production  are  present  in  many  instances. 

Attacks  of  palpitation  and  cardiac  distress  are  of  frequent  oc- 
currence, and  are  apt  to  be  excited  and  exaggerated  by  emotion, 
exposure  to  cold,  etc.  The  inability  of  the  heart  to  cope  w-ith  the 
circulatory  difficulties  is  shown  also  by  rapid  and  laboured  breathing, 
cough,  etc.,  and  sometimes  by  attacks  of  dyspnoea,  which  may 
culminate  in  convulsions. 

Inflammatory  affections  of  the  lungs,  hemoptysis,  and  tubercular 
disease  are  likewise  predisposed  to  by  the  continued  derangement  of 
the  pulmonic  circulation. 

The  nervous  and  digestive  systems  are  not  exempt  from  the  effects 
of  the  general  circulatory  incompetence. 


CONGENITAL  AFFECTIONS  OF  THE  HEART       1 1 1 

Cerebral  hsemorrhage,  attacks  of  convulsions  or  unconsciousness, 
lethargy  of  mind,  gastric  and  intestinal  disturbances,  are  often 
referable  to  interference  with  the  blood  supply  of  these  systems. 

The  temperature  of  the  internal  parts  is  usually  normal,  while 
that  of  the  surface  of  the  body  is,  as  a  rule,  considerably  lowered,  in 
consequence,  no  doubt,  of  the  loss  of  heat  by  the  dilated  capillaries 
and  the  sluggish  circulation  through  them. 

PHYSICAL  SIGNS 

Physiognomy  and  general  appearance. — The  aspect  and  general 
appearance  of  the  patient,  which  in  the  large  majority  of  cases  is 
highly  suggestive  of  insufficient  aeration  of  the  blood,  has  already 
been  described. 

Gibson  has  recently  called  attention  to  the  remarkable  concentra- 
tion of  the  blood  which  obtains  in  cases  of  congenital  disease  of  the 
heart.  Examination  shows  an  increase  in  the  specific  gravity,  as  well 
as  in  the  hsemoglobin  and  corpuscular  ingredients  of  the  blood. 
Gibson  attributes  the  condition  to  the  lessened  wear  and  tear  of 
the  red  blood  cells,  consequent  on  the  diminished  metabolism  that 
takes  place  with  venous  stasis. 

Pulse. — The  pulse  does  not  present,  as  a  rule,  any  features  of 
special  interest.  It  is  frequently  irregular  both  in  force  and  fre- 
quency, and  these  characters  are  especially  noticeable  during  the 
attacks  of  palpitation  to  which  the  subjects  of  congenital  disease  of 
the  heart  are  liable.  In  cases  of  pulmonic  stenosis  the  size  and 
strength  of  the  pulse  are  said  to  be  of  service  in  the  determination 
of  the  condition  of  the  interventricular  septum.  Thus  if  the  pulse  be 
small  in  the  radial  artery,  the  inference  is  that  the  supply  of  blood  to 
the  left  ventricle  is  diminished,  and  hence  the  septum  is  perfect. 

On  the  other  hand  if  the  pulse  in  the  radial  artery  be  of  normal 
volume  and  strength,  the  inference  is  that  the  supply  of  blood  to  the 
left  ventricle  is  supplemented  from  some  other  source,  and  hence  the 
probability  of  the  existence  of  an  imperfect  septum  ventriculorum. 

The  tone  of  the  arterial  system  is,  generally  speaking,  below  par. 

Heart. — Inspection  commonly  reveals  prominence  or  bulging  of 
the  chest  wall  in  the  prascordial  area,  involving  the  lower  part  of  the 
sternum  and  third,  fourth,  and  fifth  left  costal  cartilages  and  inter- 
costal spaces. 

Pulsation  is  often  visible  in  these  situations,  but,  as  a  rule,  is  most 
marked  in  the  epigastrium. 

The  cardiac  impulse  is  forcible  and  displaced  outwards. 

A  thrill  systolic  in  time  is  sometimes  palpable  over  the  base  of  the 
heart  at  or  about  the  level  of  the  second  left  intercostal  space. 

Percussion  may  demonstrate  an  increase  in  the  area  of  cardiac 
dulness,  either  to  the  right  or  left  of  its  normal  limits. 

The  auscultatory  phenomena  depend  on  the  site  and  nature  of  the 
lesion. 


112  DISEASES  OF  THE  HEART 

Pulmonary  stenosis  gives  rise  to  a  loud  blowing  systolic  murmur, 
which  is  most  distinctly  heard  over  the  second  left  costal  cartilage, 
though  in  many  instances  it  is  audible  over  the  greater  portion  of  the 
prsecordial  area.  The  second  sound  may  be  weak  or  accentuated, 
and  is  sometimes  accompanied  or  followed  by  a  diastolic  bruit. 

Patency  of  the  ductus  arteriosus  is,  in  all  probability,  indicated  by 
a  loud  rumbling  systolic  murmur,  most  clearly  audible  at  or  slightly 
to  the  left  of  the  pulmonic  cartilage,  in  conjunction  with  accentua- 
tion of  the  pulmonary  second  sound. 

Deficiency  of  the  interventricular  septum  occasions  a  very  loud 
and  more  or  less  musical  systolic,  or  sometimes  nearly  continuous 
bruit,  which  is  very  commonly  audible  over  the  greater  portion  of 
the  chest.  The  characteristic  feature  of  the  murmur  is  that  it  is 
heard  most  distinctly  along  the  course  of  the  interventricular  septum 
and  rapidly  diminishes  in  intensity  as  the  stethoscope  leaves  this  line 
(Maguire). 

The  direction  of  the  interventricular  septum  is  approxim.ately 
shown  by  a  line  drawn  from  the  second  left  costal  cartilage  at  its 
junction  with  the  sternum  to  a  point  about  half  an  inch  inside  the 
apex  beat.  So  far  as  is  known,  deficiency  of  the  interauricular 
septum  in  the  form  of  patent  foramen  ovale  gives  n'&t  per  se  neither 
to  symptoms  nor  physical  signs  of  any  importance. 

The  physical  signs  produced  by  congenital  lesions  at  the  aortic 
orifice  do  not  differ  from  those  found  in  association  with  the  similar 
acquired  forms  of  disease  at  this  orifice. 

DIAGNOSIS 

The  differential  diagnosis  of  congenital  and  acquired  disease  of 
the  heart  seldom  presents  much  difficulty,  provided  a  careful  con- 
sideration be  given  to  the  history  and  physical  signs  of  the  case,  in- 
cluding an  examination  of  the  blood. 

The  diagnosis  of  the  precise  nature  of  the  congenital  defect,  or 
defects,  is  a  much  more  complicated  problem,  and  one  that  in  many 
instances  it  is  impossible  to  elucidate. 

Very  extensive  cardiac  malformations  are  usually  incompatible 
with  the  duration  of  life  for  more  than  a  few  hours  or  days,  hence, 
except  during  the  earliest  periods  of  extra-uterine  life,  the  differential 
diagnosis  of  congenital  lesions  of  the  heart  is  restricted  within  com- 
paratively narrow  limits. 

From  a  clinical  point  of  view,  chief  interest  centres  in  the  diagnosis 
of  pulmonary  stenosis,  since  in  the  immense  majority  of  cases  this 
lesion  is  found  in  patients,  presenting  a  history  of  cyanosis  from 
the  time  of  birth  in  association  with  other  indications  of  a  malformed 
heart,  who  have  survived  the  twelfth  year  (Peacock).  If,  therefore, 
in  a  patient  over  twelve  years  of  age,  with  a  history  of  cyanosis  since 
birth,    there   is   evidence   of  enlargement  of  the  right  ventricle  in 


CONGENITAL  AFFECTIONS  OF  THE  HEART       113 

addition  to  the  presence  of  a  systolic  bruit  in  the  pulmonic  area, 
which  is  not  conducted  up  into  the  neck,  a  diagnosis  of  pulmonary 
stenosis  is  certainly  justifiable. 

The  presence  or  absence  of  associated  deficiency  of  the  inter- 
auricular  or  interventricular  septum,  or  of  an  open  state  of  the  ductus 
arteriosus,  or  of  some  combination  of  these  conditions,  cannot,  as  a 
rule,  be  determined  with  any  degree  of  certainty.     (See  p.  in.) 

Since  patency  of  the  foramen  ovale  is  unaccompanied  by  any 
known  symptoms  or  physical  signs,  the  question  of  the  presence  or 
absence  of  this  anomaly  does  not  require  any  further  consideration. 

Deficiency  of  the  interventricular  septum  will  be  indicated  by 
enlargement  of  both  ventricles  and  by  the  presence  of  a  systolic,  or 
of  a  more  or  less  continuous  murmur,  which  can  be  heard  most 
distinctly  in  the  mid-sternal  region  and  along  the  course  of  the  inter- 
ventricular septum. 

A  murmur  having  these  characters  should  suffice  to  distinguish 
deficiency  of  the  interventricular  septum  occurring  as  an  independent 
lesion  from  other  forms  of  congenital  disease  of  the  heart. 

If,  in  association  with  the  symptoms  and  signs  of  pulmonic 
stenosis,  the  amount  of  hypertrophy  of  the  right  ventricle  were  much 
greater  than  the  degree  of  pulmonary  narrowing,  estimated  on  other 
grounds,  would  account  for,  the  existence  of  a  patent  condition  of 
the  ductus  arteriosus  may  be  suspected.  This  suspicion  would  be 
strengthened  by  the  presence  of  accentuation  of  the  pulmonic  second 
sound. 

The  symptoms  and  signs  of  congenital  affections  of  the  other 
cardiac  orifices  and  valves  do  not  call  for  special  comment,  inasmuch 
as  they  resemble  for  the  most  part  those  found  in  connection  with 
similar  lesions  of  acquired  origin.  Nevertheless,  it  must  be  borne 
in  mind  that  the  frequent  concurrence  of  two  or  more  congenital 
anomalies  of  the  heart  must  of  necessity  lead  to  more  or  less  over- 
lapping and  modification  of  the  symptoms  and  signs  due  to  the 
respective  lesions. 

Transposition  of  the  great  vessels  is  sometimes  found  in  associa- 
tion with  transposition  of  the  heart  and  other  viscera,  but  per  se  this 
abnormality  does  not  give  rise  to  any  diagnostic  symptoms  or  signs. 

PROGNOSIS 

Dextro-cardia,  meso-cardia,  small  openings  in  the  septa  of  the 
heart,  and  malformations  of  the  valves  exercise  but  little  influence 
on  the  ordinary  expectancy  of  life,  except  in  so  far  as  the  lasi- 
mentioned  condition  may  predispose  to  the  incidence  of  inflam- 
matory affections  of  these  structures. 

Moderate  stenosis  of  the  trunk  or  orifice  of  the  pulmonary  artery, 
without  other  malformation,  but  with  adequate  compensatory  hyper- 
trophy of  the  right  ventricle,  is  compatible  with  the  enjoyment  of 
1 


114  DISEASES   OF   THE    HEART 

many  years  of  healthy  Hfe,  and  old  age  has  more  than  once  been 
attained  under  these  conditions. 

In  point  of  fact,  if  the  unimportant  lesions  mentioned  above  be 
excluded,  the  prognosis  in  uncomplicated  pulmonary  stenosis  is  more 
favourable  than  in  any  other  form  of  congenital  cardiac  affection. 

If  patency  of  the  foramen  ovale  is  combined  with  narrowing  of 
the  pulmonic  orifice,  apart  from  the  fact  that  this  association  usually 
implies  a  greater  degree  of  stenosis  of  the  arterial  opening,  the 
expectancy  of  life  is  materially  curtailed.  Nevertheless,  in  excep- 
tional cases  of  this  kind  the  patient  has  reached  middle  life,  but,  as 
a  rule,  the  age  at  death  seldom  exceeds  fifteen  or  twenty  years. 

The  duration  of  life  is  still  further  reduced  if  the  pulmonic 
narrowing  is  associated  with  deficiency  of  the  interventricular 
septum,  for  under  these  conditions  the  patient  seldom  reaches  the 
age  of  puberty. 

If  the  pulmonic  lesion  is  combined  with  an  open  state  of  the 
ductus  arteriosus,  life  is  rarely  prolonged  beyond  the  thirteenth  year. 

When  the  pulmonary  orifice  or  artery  is  completely  impervious, 
the  patient  does  not,  as  a  rule,  survive  the  first  two  or  three 
years. 

With  regard  to  stenosis  of  the  aortic  orifice,  the  prospect  of  life 
depends  largely  on  the  degree  of  narrowing,  and  on  the  concomitant 
lesions.  If  the  stenosis  has  been  sufficient  to  establish  patency  of 
the  interventricular  septum,  life  is  seldom  prolonged  beyond  the 
tenth  year. 

When  the  heart  consists  of  one  ventricle,  with  a  double  or  single 
auricle,  the  expectation  of  life  can  usually  be  expressed  in  days 
rather  than  years,  although  a  few  cases  are  recorded  of  survival 
beyond  infancy. 

Transposition  of  the  aorta  and  pulmonary  artery  is  incompatible 
with  any  lengthened  period  of  existence.  Patency  of  the  ductus 
arteriosus  is  usually  combined  with  stenosis  of  the  pulmonic  or 
aortic  orifice.  The  prognosis  in  these  cases  depends  largely  on  the 
degree  of  narrowing  which  obtains  at  the  arterial  openings.  When 
patency  of  the  ductus  arteriosus  occurs  as  an  independent  lesion, 
it  does  not  appear  to  have  a  very  unfavourable  influence  on  the 
duration  of  life,  since  the  subjects  of  this  malformation  have  in 
several  instances  reached  middle  age. 

Patent  foramen  ovale  does  not  per  se  seriously  interfere  with  the 
duration  of  life. 

During  infancy  the  cause  of  death  is  frequently  traceable  to 
mechanical  interference  with  the  circulation.  A  large  num.ber  of 
the  subjects  of  congenital  cardiac  disease  die  from  cerebral  or 
pulmonary  complications. 

If  the  patient  reaches  adult  life,  the  most  common  cause  of  death 
is  tubercular  disease  of  the  lungs.  In  some  instances  the  fatal 
termination  is  brought  about  by  cardiac  failure. 


CONGENITAL  AFFECTIONS  OF  THE  HEART    115 


TREATMENT 

The  treatment  of  congenital  affections  of  the  heart  should  be 
conducted  on  the  general  principles,  which  will  be  considered  in 
some  detail  under  the  section  dealing  with  the  acquired  varieties  of 
morbus  cordis.  It  will  therefore  be  unnecessary  here  to  give  more 
than  a  brief  resume  of  the  treatment  that  is  especially  applicable  to 
congenital  heart  disease. 

It  has  already  been  pointed  out  that  the  symptoms  are  referable, 
for  the  most  part,  to  disturbance  of  the  circulation.  All  measures, 
therefore,  which  increase  the  effectiveness  of  the  heart's  action,  or 
relieve  obstruction  to  the  onward  flow  of  blood,  have  their  thera- 
peutic value  in  the  treatment  of  congenital  disease  of  the  heart. 

Hygienic  treatment,  which  is  of  the  first  importance,  comprises 
rest,  the  avoidance  of  excitement  or  exertion,  warmth,  fresh  air,  and 
a  carefully  regulated  diet.  All  conditions  liable  to  induce  bronchial 
irritation  should  be  sedulously  avoided.  Careful  protection  against 
cold,  and  the  adoption  of  an  open-air  life,  would  go  far  to  counter- 
act the  liability  to  pulmonary  tuberculosis  that  is  observed  after 
adult  age  is  reached. 

Recourse  may  be  had  to  massage,  with  the  object  not  only  of 
relieving  superficial  congestion  and  of  assisting  the  onward  flow  of 
blood,  but  also  of  restoring  tone  to  the  tissues  and  bloodvessels 
without  the  intervention  of  active  exercise. 

Medicinal  treatment,  except  in  so  far  as  depletion  of  the  vascular 
system  can  be  accomplished  by  saline  purgatives  and  diuretics, 
consists  in  the  careful  exhibition  of  cardiac  tonics  and  in  the  relief 
of  complications. 

DigitaHs  must  be  used  with  caution,  but  under  suitable  conditions 
it  is  often  of  great  service,  more  especially  in  combination  with 
strychnine. 

Hypodermic  injections  of  ether  are  of  value  when  the  use  of 
digitalis  is  contra-indicated. 

Attacks  of  dyspnoea  and  palpitation,  which  are  often  very  trouble- 
some at  night,  may  be  treated  by  the  compound  spirits  of  ether,  by 
camphor  and  spirits  of  chloroform,  or  by  alcohol,  in  the  form  of 
whisky  or  brandy.  In  urgent  cases  of  this  kind,  and  in  convulsive 
seizures,  relief  may  be  obtained  by  the  direct  abstraction  of  blood, 
which  can  be  effected  by  means  of  leeches,  or  by  venesection.  It 
must  not,  however,  be  forgotten  that  removal  of  blood,  except  in 
very  small  quantity,  is  not  well  borne  by  the  subjects  of  congenital 
disease  of  the  heart. 


CHAPTER   Vn 
DISEASES    OF   THE    PERICARDIUM 

Classification — Section  I.  Acute  Pericarditis — Section  II.  Pericardial  Adhesion — 
Section  III.  Hydropericardium — Section  IV.  Hsemopericardium — Section  V. 
Pneumopericardium — Section  VI.  New  Growths. 

The  morbid  conditions  which  may  effect  the  pericardium  will  be 
considered  under  the  following  arrangement : — 

1.  Acute  pericarditis 

2.  Pericardial   adhesion    (including   chronic   pericarditis,  ex- 

ternal pericarditis,  etc.) 

3.  Hydropericardium 

4.  Hsemopericardium 

5.  Pneumopericardium 

6.  New  growths 

SECTION    1 

ACUTE    PERICARDITIS 

^ETIOLOGY 

Acute  inflammation  of  the  pericardium  occurs  most  commonly  in 
association  with  rheumatism  and  Bright's  disease,  and  is  found 
about  twice  as  frequently  in  connection  with  the  former  as  with  the 
latter  disorder. 

As  a  rule  it  appears  early  in  rheumatism  and  late  in  Bright's 
disease,  and  is  a  much  less  fatal  complication  of  the  one  than  of 
the  other. 

Pericarditis  sometimes  arises  in  the  course  of  enteric  fever, 
scarlatina,  measles,  small-pox,  septicaemia,  and  pyaemia.  It  may 
occur,  too,  as  the  result  of  the  extension  of  an  inflammatory  or 
other  morbid  process  from  neighbouring  structures,  such  as  the 
heart ;  pleurae,  lungs,  mediastina,  and  their  glands  ;  liver ;  stomach ; 
peritoneum,  etc.  It  is  occasionally  due  to  direct  mechanical  injury, 
as,  for  instance,  may  be  caused  by  a  blow  in  the  prsecordial  area. 
Inflammation  of  the  pericardium  is  not  infrequently  associated  with 
pneumonia,  especially  in  children.  In  this  connection  the  pericardial 
affection  may  be  due  to  the  extension  of  the  inflammatory  process 
from  the  lungs,  or  to  toxsemic  causes. 

Among  the  many  micro-organisms  which  are  found  in  connection 
with  pericarditis  may  be  mentioned  streptococci,  staphylococci, 
micrococci,  pneumococci,  gonococci,  tubercle  bacilli  and  the  bacillus 
coli  communis. 

116 


DISEASES    OF   THE    PERICARDIUM  117 

Tubercular  pericarditis  may  arise  in  several  ways.  Thus  the 
pericardium  may  be  attacked  in  common  with  the  other  serous 
membraneSj  such  as  the  pleurae  or  peritoneum,  or  it  may  become 
involved  as  part  of  the  manifestation  of  a  general  tuberculosis. 

Again,  the  implication  of  the  pericardium  sometimes  depends  on 
the  extension  of  tubercular  disease  affecting  the  pleurae  or  neigh- 
bouring lymphatic  glands.  Pericarditis  due  to  cancer  arises  in  a 
similar  way.  It  occasionally  happens  that  inflammation  of  the 
pericardium  occurs  in  the  absence  of  any  ascertainable  cause,  and 
in  such  instances  it  is  termed  "idiopathic."  In  a  few  cases 
pericarditis  has  been  attributed  to  exposure  to  cold  and  pro- 
longed exertion. 

PATHOLOGY  AND  MORBID  ANATOMY 

The  morbid  process  commences  with  an  acute  hypersemia  of 
the  pericardial  vessels,  accompanied  by  increased  exudation.  The 
membrane  becomes  swollen,  owing  to  infiltration  by  inflammatory 
effusion,  and  its  surface  appears  injected,  dull,  and  somewhat 
roughened  by  reason  of  the  deposition  upon  it  of  fibrinous  material. 
The  inflammatory  process  may  not  advance  beyond  this  stage 
(pericarditis  sicca),  but  more  commonly  it  goes  on  to  the  effusion 
of  a  variable  quantity  of  fluid  into  the  pericardial  sac,  from  which 
fibrin  is  precipitated  on  to  the  opposed  surfaces  of  the  membrane. 

The  fibrinous  deposit  is  sometimes  locahzed,  but,  as  a  rule,  it 
tends  to  spread  generally,  in  consequence  of  the  movements  of  the 
heart.  It  appears  in  the  form  of  layers  of  yellowish  lymph,  which, 
in  the  early  stages  of  the  inflammatory  process,  is  but  loosely 
applied  to  the  subjacent  membrane,  and  may  often  be  stripped  off 
in  concentric  laminae,  leaving,  on  removal,  a  smooth  surface. 

Owing  to  the  rubbing  together  of  the  opposed  sides  of  the 
membrane,  caused  by  the  movements  of  the  heart,  the  two  lymph- 
lined  pericardial  surfaces  become  remarkably  roughened,  and  present 
a  variety  of  appearances  which  are  often  described  as  papilliform, 
shaggy,  honeycombed,  etc. 

The  amount  of  fibrin  deposited  and  of  fluid  effused  is  subject  to 
considerable  variation. 

The  effusion  may  be  sero-fibrinous  or  purulent,  and  is  sometimes 
blood-stained.  In  rheumatic  pericarditis  it  is  almost  invariably  sero- 
fibrinous. The  fluid  is  not  infrequently  stained  with  blood  in 
tubercular  and  cancerous  cases,  and  this  is  ordinarily  the  case  when, 
as  rarely  happens,  pericarditis  complicates  scurvy  or  other  blood 
disorders,  such  as  purpura,  etc. 

Purulent  effusion  is  usually  associated  with  pyaemic  conditions, 
but  it  may  be  observed  in  connection  with  Bright's  disease. 
Purulent  effusion  is  more  common  in  children  than  in  adults. 

Sero-fibrinous  effusions  tend  sooner  or  later  to  become  absorbed, 
and  the  visceral  and  parietal  layers  of  the  pericardium  come  again 


ii8  DISEASES   OF   THE    HEART 

into  contact  and  temporarily  adhere.  This  temporary  adhesion 
between  the  two  layers  of  the  pericardium  may  become  permanent 
by  virtue  of  the  absorption  and  organization  of  the  fibrinous 
deposit  on  the  opposed  surfaces  of  the  membrane.  The  attach- 
ments thus  formed  may  be  partial  or  complete.  In  the  first  event 
a  general  or  local  thickening  of  the  membrane  with  a  few  scattered 
adhesions  between  the  parietal  and  visceral  layers  may  be  the  sole 
expression  of  a  past  pericarditis,  while  in  the  second  the  two 
opposed  surfaces  become  universally  adherent,  and  the  pericardial 
cavity  is  obliterated. 

In  extreme  cases  of  this  kind  the  heart  appears  enveloped  in 
a  thick  fibrous  covering,  which  in  a  few  instances  has  undergone  a 
further  calcareous  transformation. 

When  the  effusion  is  purulent  the  inflammatory  changes  are  more 
obvious,  and  the  pericardial  sac  becomes  filled  with  a  yellowish 
pus,  which  sometimes  contains  micro-organisms  (see  p.  ii6). 

In  rare  instances  a  purulent  effusion  dries  up  into  one  or  more 
caseous  masses,  which  become  intersected  by  fibrous  adhesions, 
and  may  ultimately  be  absorbed  or  converted  into  calcareous 
material.  Such  a  termination  is,  however,  exceptional,  since  these 
cases  usually  end  fatally. 

Pericarditis  is  almost  invariably  accompanied  by  a  certain  degree 
of  myocarditis,  in  consequence  of  the  direct  extension  of  the 
inflammatory  process  to  the  walls  of  the  heart,  the  outermost  layers 
of  which  become  softened,  and  undergo  fatty  changes.  The  parts 
thus  affected  may  ultimately  atrophy,  and  be  replaced  by  fibrous 
tissue.  Apart  from  extension,  myocarditis,  frequently  accompanies 
pericarditis,  the  two  affections  being  the  result  of  a  common  cause. 
In  rheumatic  cases  the  pericardium,  myocardium,  and  endocardium, 
are  not  infrequently  simultaneously  involved  in  inflammatory  changes. 
a  condition  of  the  heart  which  may  be  appropriately  described,  after 
Sturges,  as  "carditis." 

The  inflammatory  changes  in  pericarditis,  may  also  extend  to  the 
outer  or  fibrous  coat  of  the  pericardium,  and  involve  the  pleurae 
and  mediastinal  tissues  (pericarditis  externa).  By  this  means  fibrous 
adhesions  may  be  formed  between  the  pericardium  and  sternum, 
and  along  the  course  of  the  great  vessels  at  the  base  of  the,  heart. 

THE  EFFECTS  OF   PERICARDITIS  ON  THE  HEART, 
GREAT  VESSELS,  AND  SURROUNDING  STRUCTURES 

Accumulation  of  fluid  in  the  pericardial  cavity  must  necessarily 
interfere  with  the  free  movement  of  the  heart,  and  this  statement 
applies  especially  to  the  diastolic  expansion  of  the  various  chambers, 
which  is  seriously  impeded  when  the  effusion  is  considerable. 
The  supply  of  blood  to  the  organ  may  be  impeded  in  consequence 
of  pressure  on  the  superior  vena  cava  and  left  innominate  vein. 

A  very  large  effusion  may  give  rise  to  displacement  and  com- 


DISEASES    OF   THE    PERICARDIUM         119 

pression  of  the  left  lung  in  the  neighbourhood  of  the  heart,  and 
in  addition  to  pressure  effects  on  the  trachea,  oesophagus,  and 
recurrent  laryngeal  nerves. 

Dilatation  of  the  heart,  more  especially  of  its  right  side, 
frequently  follows  the  myocardial  inflammation  associated  with 
pericarditis,  and  is  due  to  the  relative  insufficiency  of  the  weakened 
cardiac  walls.  The  process  may  be  perpetuated,  and  is  no  doubt 
sometimes  initiated,  by  pericardial  thickening  and  adhesion,  which 
operate  by  hampering  the  movements  of  the  heart,  and  thus 
increasing  its  work,  and  also  by  inducing  muscular  atrophy  through 
pressure  on  the  myocardium. 

At  the  same  time  pericardial  adhesion,  even  when  extensive, 
does  not  invariably  give  rise  to  enlargement  of  the  heart. 

Pericardial  adhesion  never  leads  directly  to  cardiac  hypertrophy, 
but  it  may  do  so  indirectly  by  producing  dilatation  of  the  organ. 

SYMPTOMS 

The  symptoms  of  pericarditis  vary  greatly  in  different  cases.  As 
a.  rule  they  are  not  very  well  marked  or  distinctive,  and  at  times, 
as  in  renal  pericarditis,  they  may  be  altogether  absent.  It  frequently 
happens,  too,  that  when  inflammation  of  the  pericardium  occurs  in 
association  with  acute  disorders,  such  as  pneumonia  or  rheumatic 
fever,  the  symptoms  are  masked  by  those  of  the  primary  disease. 

The  onset  of  pericarditis  is  shown  in  some  instances  by  a  general 
exacerbation  of  the  symptoms  of  the  previously  existing  disorder. 
Occasionally  inflammation  of  the  pericardium  commences  with  a 
rigor,  which  is  followed  by  a  variable  degree  of  pyrexia.  At  other 
times  the  disease  begins  insidiously,  and,  unless  repeated  examination 
of  the  heart  be  made,  may  be  entirely  overlooked. 

Pain,  which  may  be  very  severe,  is  usually  an  early  and  prominent 
symptom,  and  is  felt  in  the  prsecordial  and  epigastric  regions,  and 
may  radiate  widely  over  the  thorax  and  upper  extremities. 

Tenderness  is  sometimes  complained  of  in  the  same  situations. 
There  is  commonly  a  feeling  of  tightness  or  oppression  at  the  chest, 
accompanied  by  cough  and  shortness  of  breath,  which  becomes 
more  pronounced  as  effusion  takes  place. 

Palpitation  may  be  a  source  of  great  distress  to  the  patient. 

All  the  symptoms  of  fever  are  usually  present.  The  temperature 
is  raised,  the  tongue  furred  ;  there  is  thirst,  loss  of  appetite,  and  the 
bowels  are  generally  constipated.  The  urine  is  scanty,  high  coloured, 
and  may  throw  down  an  abundant  deposit  of  urates.  It  sometimes 
contains  albumen. 

As  the  accumulation  of  fluid  in  the  pericardial  sac  increases, 
many  of  these  symptoms  are  intensified.  The  breathing  becomes 
increasingly  difficult  and  laboured,  so  that  the  patient  has  to  be 
propped  up  in  bed,  though  in  some  instances  of  extensive  effusion 
the  decubitus  is  dorsal,  since  any  attempt  to  raise  the  head  tends  to 


I20  DISEASES   OF   THE    HEART 

increase  the  cerebral  ansemia,  and  hence  to  cause  faintness.  The 
shortness  of  breath  may  become  so  great  that  the  patient  can 
hardly  speak,  and  with  the  dyspnoea  there  is  often  a  short,  hacking, 
troublesome  cough.  Paroxysmal  attacks  of  dyspnoea  are  occasionally 
observed. 

The  face  is  ashy  pale,  the  features  drawn  and  anxious,  and  the 
movements  of  the  alse  nasi  plainly  visible.  The  trunk  is  usually 
kept  perfectly  still,  while  the  head  and  arms  are  moved  restlessly 
about. 

With  extensive  effusions  pressure  effects  on  neighbouring  structures 
may  be  observed. 

Pain  or  difficulty  in  swallowing  is  due  to  pressure  upon  the 
oesophagus,  though  it  has  occasionally  been  ascribed  to  nerve 
irritation. 

Irritation  of  the  recurrent  laryngeal  or  phrenic  nerves  from 
pressure,  or  from  implication  in  the  inflammatory  process,  may  give 
rise  to  aphonia  or  hiccough. 

Compression  and  collapse  of  the  base  of  the  left  lung  are' 
occasionally  observed,  and  are  a  source  of  additional  respiratory 
distress. 

The  return  of  blood  to  the  heart  may  be  impeded  by  pressure  on 
the  great  venous  trunks  in  the  thorax,  and  the  veins  in  the  neck  are 
not  infrequently  distended  from  this  cause.  Thrombosis  has  been 
known  to  occur  in  the  left  innominate  vein  in  cases  of  pericardial 
effusion,  and  is  an  event  that  would  add  greatly  to  the  congestion  of 
the  veins  of  the  head,  neck,  and  upper  extremities. 

Dropsy  is  sometimes  observed,  and  may  be  due  to  venous  stasis 
or  to  myocardial  weakness,  or,  as  more  commonly  happens,  to  a 
combination  of  these  conditions. 

Cerebral  symptoms  in  the  form  of  headache,  sleeplessness,  and 
slight  delirium  are  not  uncommon. 

Vomiting,  said  to  be  of  nervous  origin,  is  sometimes  a  prominent 
feature  of  acute  pericarditis. 

Serious  delirium,  convulsions,  coma,  etc.,  have  been  noted, 
chiefly  in  rheumatic  cases,  but  they  are  of  rare  occurrence. 

The  symptoms  of  pericarditis  in  children  are  even  more  indefinite 
than  in  adults.  The  onset  of  the  disease  is  often  very  insidious  in 
young  people.  An  increase  in  the  pulse  rate,  and  an  irregular  and 
excited  action  of  the  heart  in  association  with  dyspnoea,  slight  fever, 
and  restlessness  should  always  lead  to  a  suspicion  of  pericarditis 
in  the  case  of  a  child  with  a  rheumatic  history.  Indeed,  in  any 
event,  the  occurrence  of  these  symptoms  during  infancy  and  early  life 
calls  for  a  careful  examination  of  the  heart,  which  should  be  repeated 
from  day  to  day. 

Acute  pericarditis  runs  a  very  variable  course.  The  ordinary 
duration  of  the  disease  is  from  ten  days  to  a  fortnight,  but  it 
occasionally  terminates  in  three  or  four  days,  and  not  uncommonly 
lasts  for  three  weeks  or  more.     It  sometimes  happens  that  an  acute 


DISEASES   OF   THE   PERICARDIUM         121 

onset  is  succeeded  by  sub-acute  inflammatory  changes,  which  run  an 
insidious  and  protracted  course. 

Acute  pericarditis  usually  terminates  in  recovery  so  far  as  the 
immediate  issue  of  the  disease  is  concerned,  but  in  a  large  number 
of  instances  the  heart  is  permanently  crippled,  to  a  greater  or  less 
extent,  by  the  organic  changes  which  are  left  behind. 

Recovery  in  cases  of  slight  or  moderate  intensity  may  be  rapid 
and  complete,  but  if  there  has  been  much  effusion  absorption  is 
usually  slow,  and  for  some  time  after  the  attack  there  is  a  tendency 
to  dyspnoea,  palpitation,  and  other  signs  of  cardiac  weakness,  when 
any  exertion  is  undertaken. 

Death,  when  it  occurs,  may  be  due  to  heart  failure,  asphyxia, 
or  exhaustion,  or  to  some  complication  of  the  disease  with  which 
the  pericardial  inflammation  is  associated. 

PHYSICAL  SIGNS 

Pulse. — In  the  early  stages  of  the  disease  the  pulse  is  increased 
in  frequency  up  to  one  hundred  or  more  beats  per  minute,  and 
may  or  may  not  be  irregular.  As  a  rule  the  artery  can  be  felt 
between  the  beats,  and  is  easily  compressible.  Later  the  pulse 
becomes  extremely  rapid,  small,  feeble,  and  irregular  in  force  and 
frequency.  In  exceptional  instances  the  occurrence  of  pericarditis 
produces  very  little  alteration  in  the  character  and  rate  of  the 
pulse. 

A  large  pericardial  effusion  occasionally  gives  rise  to  the  pulsus 
paradoxus. 

Heart. — The  earliest  indications  of  the  roughening  of  the  opposed 
pericardial  surfaces  are  obtained  by  means  of  palpation  and  auscul- 
tation, and  consist  of  the  signs  known  as  "pericardial  friction 
fremitus"  and  "pericardial  friction  sound." 

Pericardial  friction  fremitus  is  comparatively  seldom  observed. 
It  is  most  commonly  detected  over  the  base  of  the  heart,  but  it 
may  be  felt  at  the  apex  and  in  this  situation  only.  Its  area  of 
production  is  usually  small,  and  frequently  changes  from  day  to 
day.  It  conveys  the  impression  that  it  is  produced  by  the  rubbing 
together  of  roughened  surfaces  immediately  beneath  the  hand. 
Pericardial  friction  fremitus  is  commonly  systolic  as  regards  its 
relation  to  the  cardiac  cycle,  but  it  may  have  a  to -and -fro 
rhythm,  i.e.  systolic  and  diastolic. 

It  differs  from  an  endocardial  thrill  in  that  it  has  no  definite 
"  focus  of  intensity "  (Sibson),  nor  has  it  the  peculiar  quivering 
quality  associated  with  the  latter  sign. 

Pericardial  friction  sound  is  one  of  the  earliest,  most  reliable 
and  constant  indications  of  the  initial  stage  of  acute  pericarditis. 
In  some  instances,  however,  owing  either  to  the  nature  of  the 
fibrinous  deposit  or,   as  is   more   likely,   to  myocardial  weakness, 


122  DISEASES  OF  THE  HEART 

the  sign  is  wanting  throughout  the  whole  course  of  the  disease. 
In  its  absence  the  recognition  of  the  onset  of  acute  pericarditis 
turns  on  the  history  and  symptoms  of  the  case,  and  on  the 
occurrence  of  an  excited,  irregular,  and  rapid  action  of  the  heart, 
with  which  may  be  associated  prolongation  of  the  first  sound  at 
the  apex,  or  reduplication  of  the  second  sound  at  the  base 
and  evidence  of  a  greater  or  less  degree  of  cardiac  dilatation. 
Nevertheless  a  diagnosis  of  acute  pericarditis  based  on  the  indica- 
tions just  mentioned  is  always  open  to  doubt  unless  confirmed 
by  the  presence  of  friction  sound  in  the  prsecordial  area,  and,  as 
stated  above,  this  can  be  detected  in  the  large  majority  of  instances. 

Pericardial  friction  sound  may  be  heard  over  any  part  of  the 
prfficordium,  but  it  is  most  commonly  observed  over  the  base  of 
the  heart.  Its  area  of  audibility  is,  with  few  exceptions,  limited 
to  the  praecordial  outline. 

Pericardial  friction  sound  has  usually  a  to-and-fro  rhythm,  i.e. 
systolic  and  diastolic,  but  it  may  exhibit  a  triple  rhythm,  i.e.  presys- 
tolic, systolic,  and  diastolic,  or  it  may  be  systolic,  or  diastolic  only. 

It  is  associated  with  the  movements  rather  than  with  the  sounds 
of  the  heart,  and  the  latter,  though  sometimes  obscured,  are  often 
audible  through  the  friction  sound. 

The  characters  of  pericardial  friction  sound  are  subject  to  con- 
siderable variation  in  accordance  with  the  conditions  under  which 
it  is  produced.  Thus  it  is  described  as  grazing,  rustling,  creaking, 
grating,  scraping,  etc.,  and  it  usually  conveys  the  impression  of  the 
rubbing  together  of  roughened  surfaces  situated  immediately  beneath 
the  ear. 

The  character,  rhythm,  intensity,  and  area  of  audibility  of  peri- 
cardial friction  sound  frequently  vary  from  day  to  day,  or  even 
from  hour  to  hour,  and  as  a  rule  are  markedly  modified  by  pressure 
with  the  stethoscope  in  the  prsecordial  area,  by  posture,  and  by 
the  respiratory  movements.  As  effusion  takes  place  into  the  peri- 
cardial sac  the  inflamed  and  roughened  surfaces  of  the  membrane 
become  separated  by  fluid  from  below  upwards,  with  the  result 
that  friction,  and  the  sound  produced  thereby,  occur  at  increasingly 
higher  levels,  and  in  the  course  of  time  may  be  completely  abolished. 
Nevertheless  if  a  friction  sound  is  once  heard  over  the  base  of  the 
heart  it  is  seldom  (never,  according  to  Balfour),  if  ever,  obliterated 
by  subsequent  effusion,  however  large  this  may  be. 

It  must  not  be  forgotten  that  the  disappearance  of  friction  sound 
in  the  course  of  acute  pericarditis  is  sometimes  due  to  the  occur- 
rence of  adhesion  between  the  two  layers  of  the  pericardium  without 
any  antecedent  effusion.  This  order  of  events  is  observed  more 
particularly  in  the  case  of  children. 

The  physical  signs  associated  with  pericardial  effusion  will  now 
be  considered. 

Prominence  or  bulging  of  the  precordial  region  is  not  un- 
commonly due  to  a  large  pericardial  eff'usion,  and  is  more  readily 


DISEASES   OF   THE   PERICARDIUM         123 

produced  in  children  than  in  adults  by  reason  of  the  greater 
flexibility  of  the  chest  wall  in  early  life. 

The  upward  and  forward  displacement  of  the  ribs  and  costal 
cartilages,  on  which  the  arching  of  the  prsecordium  depends,  is 
accompanied  by  a  widening  and  smoothing  out  of  the  intercostal 
spaces.  A  very  large  effusion  has  been  known  to  exaggerate  the 
normal  curvature  of  the  dorsal  portion  of  the  spinal  column 
(Sibson). 

When  the  apex  beat  of  the  heart  is  visible  it  appears  to  be  dis- 
placed upwards  together  with  the  cardiac  impulse,  which  becomes 
progressively  feebler  and  less  perceptible  as  the  effusion  and 
myocardial  debility  increase. 

According  to  some  observers,  an  undulatory  movement  can  some- 
times be  detected  in  the  prsecordial  area  in  cases  of  abundant 
effusion,  and  this  they  ascribe  to  waves  of  fluid  produced  by  the 
beating  of  the  heart.  This  interpretation  of  the  phenomenon,  if  it 
is  ever  seen,  is  disputed  by  others  who  attribute  it  merely  to  an 
enfeebled  cardiac  impulse. 

A  large  pericardial  effusion  may  give  rise  to  depression  of  the 
diaphragm  and  liver,  and  by  this  means  to  prominence  of  the 
epigastrium.  Paralysis  of  the  diaphragm,  which  sometimes  occurs 
in  pericarditis,  would  be  indicated  by  inspiratory  recession  of  the 
epigastrium  and  costal  breathing. 

Interference  with  the  return  of  blood  to  the  heart  is  frequently 
shown  by  distension  of  the  large  venous  trunks  in  the  neck. 

The  position  of  the  apex  beat  and  the  character  of  the  cardiac 
impulse  are  better  appreciated  by  means  of  palpation.  The  apex 
beat  may  appear  to  be  situated  in  the  fourth  interspace  or  even 
higher,  but  the  impulse  felt  in  these  situations  is  probably  due  to 
the  impact  of  a  portion  of  the  heart  above  the  apex  against  the 
chest  wall,  the  apex  itself  being  separated  from  the  thoracic 
parietes  by  a  layer  of  fluid.  If  this  explanation  be  correct,  the 
so-called  "displacement  upwards  of  the  apex  beat"  is  apparent 
rather  than  real.  Strongly  confirmatory  of  this  view  is  the  fact 
that  the  apex  beat  may  sometimes  be  felt  in  its  normal  situation 
when  the  patient  leans  well  forwards,  a  manoeuvre  which  brings 
the  heart  nearer  to  the  chest  wall.  It  must  not  be  forgotten  that 
in  children  the  apex  beat  is  normally  situated  in  the  fourth  inter- 
space. 

Dr.  Ewart  is  of  the  opinion  that  an  alteration  in  the  relation 
between  the  left  clavicle  and  the  first  rib,  v/hich  he  terms  the 
"first  rib  sign,"  is  an  important  indication  of  a  large  pericardial 
effusion.  The  sign  consists  in  a  raising  of  the  clavicle  whereby  the 
upper  edge  of  the  first  rib  can  be  felt  as  far  forwards  as  its  sternal 
attachment. 

An  increase  in  the  area,  and  an  alteration  in  the  shape  of  the 
normal  cardiac  dulness,  are  signs  of  the  first  importance  in  the 
diagnosis  of  pericardial  effusion. 


124  DISEASES    OF   THE    HEART 

With  the  patient  in  the  recumbent  position  the  increase  of  dul- 
ness  is  first  observed  at  the  base  of  the  heart  in  the  neighbourhood 
of  the  great  vessels,  where  the  pericardial  sac  is  easily  distensible. 
In  the  early  stages  of  the  effusion  the  dulness  extends  upwards  as 
high  as  the  second  or  first  rib  on  the  left  side,  and  laterally  for 
about  an  inch  to  an  inch  and  a  half  outside  the  left  sternal  edge. 
As  the  fluid  increases  it  dilates  the  pericardial  sac  round  the  heart 
itself  and  gravitates  towards  the  oiost  dependent  part  of  the  cavity. 
The  area  of  dulness  now  assumes  a  pyriform,  or  roughly  triangular 
outline,  with  the  base  of  the  figure  downwards.  Laterally,  in 
extreme  instances,  it  may  extend  from  the  right  nipple  line  to  the 
left  axillary  line,  and  upwards  it  may  reach  as  high  as  the  episternal 
notch. 

Rotch  concludes,  as  the  result  of  the  artificial  injection  of  fluid 
into  the  pericardium,  that  a  pericardial  effusion  gravitates  from  the 
outset  to  the  lower  part  of  the  sac,  and  produces  dulness  to  the 
right  and  left  of  the  sternum  in  the  fifth  intercostal  spaces.  He 
considers  absolute  dulness  in  the  fifth  right  interspace  to  be 
diagnostic  of  pericardial  effusion,  but  this  sign  has  not  always  the 
significance  attributed  to  it  by  Rotch. 

The  area  of  dulness  varies  somewhat  with  the  position  of  the 
patient.  It  is  greater  in  the  erect  than  in  the  recumbent  posture, 
since  in  the  latter  position  the  fluid  gravitates  behind  the  heart. 
For  a  like  reason  the  line  of  dulness  may  be  made  to  move  further 
to  the  right  or  left,  according  as  the  patient  lies  on  his  right  or  left 
side. 

As  a  rule,  the  line  of  demarcation  between  the  dulness  due  to  a 
pericardial  effusion  and  the  surrounding  pulmonary  resonance  is 
exceedingly  well  defined  by  an  abrupt  change  in  the  percussion 
note,  but  it  must  be  borne  in  mind  that  the  presence  of  air- 
containing  lung  in  front  of  the  pericardium,  such  as  may  obtain 
in  cases  of  emphysema,  can  seriously  obscure  the  percussion 
dulness. 

It  occasionally  happens  that  even  a  large  pericardial  effusion  gives 
rise  to  very  little  increase  in  the  area  of  cardiac  dulness,  and  in 
such  instances  the  fluid  lies  for  the  most  part  behind  the  heart. 

The  relation  of  the  apex  beat  to  the  left  limit  of  cardiac  dulness 
should  be  carefully  explored,  for  in  many  cases  of  pericardial 
effusion  the  area  of  dulness  extends  considerably  further  to  the 
left  than  the  apex  beat. 

The  fingers  experience  a  feeling  of  increased  resistance  over  a 
pericardial  effusion,  and  it  is  frequently  possible,  by  employing  the 
method  of  procedure  advocated  by  Maguire,  to  map  out  the  outline 
of  the  distended  sac  with  the  greatest  nicety  by  means  of  palpation 
alone. 

It  was  originally  pointed  out  by  Bamberger,  and  his  observations 
have  since  been  confirmed  by  others,  that  a  considerable  pericardial 
effusion  may  give  rise  to  a  well-defined  area  of  percussion  dulness, 


DISEASES  OF  THE  PERICARDIUM  125 

about  the  size  of  a  five-shilling  piece,  in  the  immediate  neighbour- 
hood of  the  angle  of  the  left  scapula.  Auscultation  over  this  patch 
of  dulness  discovers  increased  vocal  fremitus,  tubular  breathing,  and 
bronchophony. 

The  auscultatory  evidence  of  pericardial  effusion  is  limited  to  the 
effect  it  produces  on  the  sounds  of  the  heart,  which  tend  to  become 
weaker  and  more  distant  as  the  fluid  increases  in  amount,  and  the 
myocardial  debility  becomes  more  pronounced. 

The  enfeeblement  of  the  sounds  is  usually  more  noticeable  at  the 
apex  than  over  the  base  of  the  heart,  where  the  second  sound  is  not 
uncommonly  reduplicated. 

A  very  large  effusion  may  render  the  sounds  altogether  inaudible 
over  any  part  of  the  prsecordium. 

The  pressure  effectsjof  a  pericardial  effusion  on  the  surrounding 
pulmonary  tissue  may  be  evidenced  by  the  signs  of  partial  con- 
solidation or  collapse  of  the  lungs,  more  particularly  of  the  left  one 
over  its  lower  lobe  posteriorly. 

During  the  process  of  absorption  of  an  inflammatory  pericardial 
effusion,  the  sounds  of  the  heart  become  more  distinct,  the  area  of 
prsecordial  dulness  gradually  diminishes,  and  friction  sound,  and 
possibly  friction  fremitus,  temporarily  reappear  as  the  surfaces  of 
the  membrane  again  come  into  contact. 

The  heart,  in  some  instances,  returns  to  its  normal  size  and 
position,  but  more  commonly  the  organ  remains  permanently  en- 
larged, in  consequence  of  the  formation  of  adhesions,  or  of  the 
effects  of  endo-  or  myocarditis. 

DIAGNOSIS 

If  pleural  and  pleuro-pericardial  causes  can  be  excluded,  the 
detection  of  friction  sound  over  any  part  of  the  prsecordial  area 
justifies  a  diagnosis  of  pericarditis,  while  the  intensity  of  the  process 
may  be  gauged  by  the  concomitant  symptoms  and  physical  signs 

The  chief  points  m  the  differential  diagnosis  of  pericardial,  pleural, 
and  pleuro-pericardial  friction  sound  have  already  been  indicated 
(see  pp.  67,  68)- 

Even  v/hen  friction  sound  cannot  be  heard,  the  occurrence  ot 
acute  pericarditis  may  still  be  recognised  by  a  careful  survey  of  the 
history,  symptoms,  and  physical  signs  presented  by  the  patient. 

In  the  absence  of  friction  sound  the  diagnosis  of  pericardial 
effusion  from  dilatation  of  the  heart,  thoracic  aneurism,  or  other 
mediastinal  tumours,  and  pleural  effusion,  has  also  to  be  considered. 

Dilatation  of  the  heart  may  closely  simulate  a  pericardial  effusion, 
and  a  combination  of  the  two  conditions,  which  is  by  no  means  un- 
common, renders  a  differential  diagnosis  almost  impossible. 

The  shape  of  the  cardiac  dulness  in  dilatation  of  the  heart  is 
usually  oval,  whereas  in  pericardial  effusion  it  is  pyriform  or  tri- 
angular. Moreover,  the  upward  extension  of  the  cardiac  dulness, 
which  is  so  marked  a  feature  of  pericardial  effusion,  seldom  rises 


126  DISEASES    OF   THE    HEART 

above  the  level  of  the  third  rib  in  cases  of  dilatation  of  the  heart. 
Furthermore,  in  dilatation  of  the  heart  the  left  lower  limit  of  dulness 
coincides  with  the  apex  beat,  while  in  a  pericardial  effusion  it 
frequently  extends  beyond  this  point.  Rotch  considers  that  abso- 
lute dulness  in  the  fifth  right  intercostal  space  close  to  the  sternum 
can  be  caused  by  pericardial  effusion  only,  but,  as  previously  pointed 
out,  this  sign  has  not  always  the  significance  attributed  to  it  by 
this  observer. 

The  aetiology,   rate  of  development,  and   symptoms  of  the  two 
conditions   also   furnish  a   means  of  distinguishing  between  them. 
Thus    pericardial   effusion   commonly   occurs   in   the   course  of   an 
attack  of  rheumatism ;  it  develops  quickly,  and  is  associated  with 
pyrexia  and  other  signs  of  febrile  disturbance.     Dilatation  of  the 
heart,  on  the  other  hand,  usually  accompanies  valvular  disease,  or 
myocardial  affections ;  as  a  rule  it  develops  slowly  (though  it  may 
do  so  rapidly),  and  in  the  absence  of  complications  does  not  give 
rise  to  fever.     It  must,  however,  be  carefully  borne  in  mind  that  a 
greater  or  less  degree  of  cardiac  dilatation  accompanies  the  large 
majority  of  cases  of  pericarditis.     Indeed,  it  is  to  the  myocardial 
involvement  that  the  chief  dangers  of  pericarditis  are  attributable. 

The  differential  diagnosis  between  thoracic  aneurism,  or  a  medi- 
astinal growth,  and  pericardial  effusion  can  generally  be  made  by 
a  careful  consideration  of  the  setiological  conditions,  the  rate  of 
development,  physical  signs,  and  pressure  effects  which  are  found 
in  association  with  the  morbid  process  that  obtains. 

The  pressure  effects  of  a  pericardial  effusion  are  seldom  very 
pronounced. 

A  large  pleural  effusion  on  the  left  side  may  give  rise  to  promi- 
nence of  the  chest  wall  in  front  of  the  heart,  and  thus  stimulate  a 
pericardial  effusion  ;  but  the  differential  diagnosis  does  not  usually 
present  any  serious  difficulty  unless  the  two  conditions  are  combined, 
when  it  is  sometimes  almost  impossible  to  distinguish  between  them, 
except  by  the  help  of  paracentesis. 

The  presence  of  pus  in  the  pericardial  sac  may  be  suspected 
when  pericarditis  complicates  pyaemia,  or  one  of  the  eruptive  fevers, 
or  when  it  follows  suppuration  in  adjacent  structures.  The  occur- 
rence of  rigors  and  elevation  of  temperature,  which  may  gradually 
assume  a  hectic  type,  and  of  other  grave  constitutional  symptoms, 
would  convert  the  suspicion  into  a  certainty.  The  physical  signs  are 
not  distinctive  of  this  condition,  though  oedema  of  the  integuments 
in  the  praecordial  region  is  more  common  in  cases  of  purulent  than 
of  simple  effusion. 


DISEASES  OF  THE  PERICARDIUM  127 


PROGNOSIS 

The  prognosis  in  acute  pericarditis  depends  mainly  on  the  nature 
of  the  primary  disorder,  and  on  the  extent  to  which  the  myocardium 
is  involved  in  the  inflammatory  process.  In  the  absence  of  previous 
myocardial  or  endocardial  mischief,  the  prognosis  in  rheumatic  cases 
is  distinctly  good.  If  the  valves  of  the  heart  have  been  injured  by 
a  previous  attack  of  rheumatism,  the  outlook  is  less  favourable. 

Pericarditis,  secondary  to  Bright's  disease,  pneumonia,  or  pyaemia, 
is  almost  invariably  fatal. 

Apart  from  these  considerations,  the  signs  of  unfavourable  import 
are  a  large  effusion,  a  rapid  and  irregular  pulse  with  a  feeble  action 
of  the  heart,  great  dyspnoea,  lividity,  and  nervous  phenomena,  such 
as  muscular  tremor,  delirium,  etc. 

Persistent  vomiting'  in  the  course  of  pericarditis  in  children  is 
of  grave  significance,  and  the  presence  of  anaemia  renders  the 
prognosis  less  favourable.  Pericarditis  is  at  all  times  a  serious 
disorder  in  young  people,  not  only  on  account  of  its  immediate 
effects  on  the  heart,  but  also  by  reason  of  the  tendency  of  the 
disease  to  recur  or  continue  in  a  sub-acute  form. 

TREATMENT 

The  first  consideration  in  the  treatment  of  acute  pericarditis  is 
the  maintenance  of  complete  rest  in  bed.  Sudden  movement  or 
exertion  of  any  kind  must  be  carefully  avoided.  The  patient 
should  be  warmly  clad  and  protected  from  draughts,  and  may,  if 
necessary,  be  propped  up  in  bed  by  means  of  suitably  arranged 
pillows. 

Light  and  easily  digestible  food  should  be  given  in  small  quantities 
at  short  and  regular  intervals. 

The  medicinal  treatment  of  acute  pericarditis  depends  in  a  large 
measure  on  the  nature  of  the  disorder  with  which  it  is  associated. 
It  is  important,  where  possible,  to  treat  the  primary  disorder  of 
which  the  pericarditis  is  but  a  local  manifestation.  Thus  rheumatism, 
the  commonest  cause  of  the  affection  under  consideration,  should, 
when  present,  be  combated  by  the  usual  remedies,  and  a  similar 
plan  of  treatment  must  be  adopted  in  the  case  of  the  other  dis- 
orders with  which  pericarditis  may  be  associated. 

Local  therapeutic  measures  are,  however,  of  the  utmost  value, 
both  as  a  means  of  relieving  pain  and  distress  and  of  mitigating  the 
severity  and  duration  of  the  inflammatory  process.  With  this  object 
the  application  of  an  ice-bag  over  the  praecordium  usually  affords 
the  most  satisfactory  results ;  but  it  is  a  method  of  treatment  which 
must  be  employed  with  caution,  especially  in  weakly  subjects,  and 
any  signs  of  cardiac  failure  should  be  met  by  the  administration 
of  digitalis  and  alcoholic  stimulants.  The  ice-bag  also  acts  as  a 
febrifuge. 


128  DISEASES  OF  THE  HEART 

Pain  may  also  be  assuaged  by  the  use  of  warm  poultices  placed 
over  the  heart,  or  by  the  hypodermic  injection  of  morphia. 

Blisters  are  sometimes  of  service,  but  they  have  the  disadvantage 
of  rendering  the  physical  examination  of  the  heart  more  difficult. 

At  the  onset  of  the  disease  a  few  leeches  applied  over  the 
praecordium  may  give  great  relief,  but  they  should  be  used  in 
robust  individuals  only. 

Whatever  plan  of  local  treatment  be  adopted,  it  ought,  as  a 
general  rule,  to  be  adhered  to  throughout  the  course  of  the  disease, 
as  the  indiscriminate  variation  of  the  different  local  apphcations  can 
only  do  harm. 

The  least  indication  of  cardiac  weakness  should  be  met  by  the 
use  of  digitalis  and  alcoholic  stimulants,  which  must  be  administered 
at  regular  intervals,  and  in  such  quantities  as  are  suitable  to  the 
requirements  of  the  case.  The  tendency  to  heart  failure  is  more 
pronounced  in  children  than  in  adults,  and  it  is  advisable  to 
anticipate  rather  than  to  wait  for  this  untoward  result  by  the  judicious 
use  of  cardiac  sedatives  and  tonics. 

One  of  the  most  useful  drugs  in  the  treatment  of  pericarditis  is 
opium.  It  relieves  pain,  quiets  the  heart,  and  promotes  sleep, 
and  in  suitable  doses  may  be  given  to  children,  though  alcohol  is 
to  be  preferred  in  the  case  of  very  young  subjects,  in  whom  its 
action  is  similar  (Cheadle). 

Venesection  is  seldom  required  in  pericarditis,  but  in  robust 
individuals,  with  the  signs  of  circulatory  embarrassment  and  engorge- 
ment of  the  right  heart,  the  abstraction  of  a  few  ounces  of  blood 
from  the  arm  sometimes  gives  great  relief. 

The  absorption  of  the  inflammatory  products  may  be  hastened 
by  the  application  of  a  few  flying  blisters  over  the  praecordium, 
or  by  the  internal  administration  of  the  iodide  of  potassium  or 
sodium,  though  the  action  of  these  remedies  for  the  purpose  in 
question  is  somewhat  uncertain. 

When  the  amount  of  fluid  effused  is  very  large,  or  when  the 
presence  of  pus  is  suspected,  the  question  of  paracentesis  has  to  be 
considered. 

The  operation  should  be  preceded  by  an  exploratory  puncture 
with  a  hypodermic  syringe  in  the  fifth  intercostal  space  on  the  left 
side,  about  an  inch  from  the  sternum,  in  order  to  confirm  the 
diagnosis.  An  aspirating  needle  is  then  introduced,  under  anti- 
septic precautions,  in  the  same  situation,  and  the  fluid  slowly  with- 
drawn. 

Rotch  suggests,  as  the  result  of  his  experiments  on  the  cadaver, 
that  the  puncture  should  be  made  in  the  fifth  right  space,  and  this 
method  of  procedure  certainly  seems  worthy  of  a  trial. 

The  operation  of  paracentesis  pericardii  is  attended  with  little  or 
no  danger,  but  care  must  be  taken  not  to  puncture  the  auricles. 

The  pericardial  cavity  has  in  a  few  instances  been  opened  by  free 
incision  and  drained,  a  procedure  which  is  essential  for  the  suc- 
cessful treatment  of  a  purulent  effusion. 


DISEASES   OF   THE    PERICARDIUM         129 

SECTION    II 
PERICARDIAL    ADHESION 

iETIOLOGY  AND   MORBID  ANATOMY 

Adhesion  between  the  two  layers  or  the  pericardium,  or  between 
the  pericardium  and  chest  wall,  is  always  of  inflammatory  origin. 
It  may  be  the  outcome  of  an  acute  or  chronic  pericarditis,  but  inas- 
much as  a  sub-acute  or  chronic  stage  of  inflammation  frequently 
follows  the  acute  process,  the  two  causes  are  not  uncommonly 
combined. 

The  distribution,  extent,  and  characters  of  the  adhesions,  which 
are  commonly  associated  with  a  greater  or  less  degree  of  pericardial 
thickening,  are  subject  to  considerable  variation. 

Thus  the  parietal  layer  of  the  pericardium  may  be  adherent  to  the 
visceral  reflection  of  the  membrane  and  heart  (endopericardial 
adhesion),  or  to  the  posterior  surface. of  the  preecordial  portion  of 
the  chest  wall  and  adjacent  structures  (exopericardial  adhesion) ;  or 
the  two  conditions  may  be,  and  frequently  are,  combined.  Exo- 
pericardial adhesion,  involving  the  great  vessels  at  the  base  of  the 
heart,  may  arise  also  in  connection  with  inflammatory  affections  of 
the  mediastinum  (pericarditis  externa,  mediastino-pericarditis,  etc.), 
pleurae,  or  contiguous  organs.  The  adhesions,  whether  endo- 
pericardial or  exopericardial,  may  be  local  or  general.  They 
appear,  at  one  time,  in  the  form  of  scattered  filamentous  threads  or 
strands,  easily  torn  through ;  while,  at  another,  they  are  found  as 
strong  fibrous  bands  or  cords,  which  are  with  difficulty  separable 
from  the  underlying  muscular  tissue  of  the  heart,  or  from  the 
posterior  surface  of  the  sternum,  as  the  case  may  be. 

When  the  myocardial  inflammation  associated  with  pericarditis 
has  been  very  extensive,  the  heart  may  appear  completely  encased 
in  a  dense  fibrous  covering,  which  sometimes,  though  rarely,  under- 
goes a  calcareous  transformation. 

The  white  opaque  patches,  commonly  termed  milk  spots,  which 
are  not  infrequently  observed  on  the  visceral  surface  of  the  peri- 
cardium, more  particularly  over  the  anterior  surface  of  the  right 
ventricle,  consist  of  a  local  thickening  of  the  serous  coat  of  the 
membrane,  and  are  due,  in  all  probability,  to  inflammatory  changes 
excited  by  friction. 

EFFECTS   ON  THE  HEART 

The  effects  of  pericardial  adhesion  on  the  heart  are  found  to  vary 
considerably.  In  about  two-thirds  of  the  cases  of  uncomplicated 
pericardial  adhesion  the  heart  is  enlarged  (Sibson),  while  in  the 
remaining  third  the  size  of  the  organ  is  either  unaltered  or 
diminished. 


I30  DISEASES   OF   THE   HEART 

The  cardiac  enlargement  is  usually  a  combination  of  hypertrophy 
and  dilatation,  but  the  latter  condition  commonly  preponderates  and 
sometimes  exists  alone. 

Though  the  whole  heart  is,  as  a  rule,  implicated  to  a  greater  or 
less  extent  in  these  changes,  the  ventricles  are  affected  much  more 
seriously  than  the  auricles,  and  the  right  side  of  the  heart  suffers 
more  than  the  left. 

The  effects  of  pericardial  adhesion  on  the  heart  are  usually 
explained  on  the  supposition  that  the  fibrous  attachments  hamper 
the  cardiac  movements,  especially  systole,  and  thus  increase  the 
work  of  the  organ,  while  its  contractile  power  is  diminished  by  the 
concomitant  myocardial  changes. 

The  influence  of  the  adhesions  in  the  production  of  cardiac 
enlargement  has  probably  been  over-estimated,  since  the  pericardium 
may  be  universally  adherent  without  giving  rise  to  any  alteration  in 
the  size  of  the  heart.  Moreover,  the  cardiac  changes  associated  with 
adherent  pericardium  are  probably  explicable  on  other  grounds. 

It  has  already  been  pointed  out  that  the  myocardium  is  usually 
more  or  less  implicated  in  the  preliminary  inflammatory  changes,  the 
effect  of  which  is  to  diminish  the  amount  of  healthy  cardiac  muscle, 
and  thus  to  render  the  heart  less  capable  of  carrying  on  the  work  of 
the  circulation.  By  this  means  a  variable  degree  of  dilatation  of  the 
heart  from  failure  is  induced,  the  intensity  of  the  process  depending 
on  the  extent  of  the  myocardial  disabiUty.  Hypertrophy  ensues  as 
a  consequence  of  the  dilatation,  but  since  the  amount  of  myocardial 
tissue  capable  of  taking  part  in  this  process  is  diminished,  to  a 
greater  or  less  extent,  the  increase  in  thickness  of  the  cardiac  walls 
is  frequently  inconsiderable,  and  may  appear  insignificant  as  com- 
pared with  that  evoked  by  an  endocardial  lesion.  The  subsequent 
formation  of  adhesions  gives  rise,  no  doubt,  to  further  cardiac 
embarrassment,  and  must  therefore  be  regarded  as  an  additional 
source  of  enlargement  of  the  heart. 

The  comparative  thinness  of  the  walls  of  the  right  ventricle  largely 
accounts  for  the  liability  of  this  chamber  to  suffer  more  from  the 
effects  of  pericardial  adhesion  than  the  left  ventricle. 

In  early  life  the  formation  of  pericardial  adhesions  may  greatly 
interfere  with  the  subsequent  growth  and  development  of  the  heart, 
and  in  this  way  may  be  a  cause  of  atrophy  of  the  organ. 

In  addition  to  the  changes  mentioned  above,  the  myocardium  is 
not  uncommonly  the  seat  of  pigmentary,  fatty,  or  fibroid  degenera- 
tion, which  may  be  the  outcome  of  the  initial  myocarditis  or  of  the 
pressure  exerted  by  the  thickened  and  adherent  pericardium  on  the 
heart  itself,  or  on  the  coronary  vessels. 

External  pericardial  adhesions  may  involve  the  great  arterial 
and  venous  trunks  at  the  base  of  the  heart,  and  sometimes  give 
rise  to  compression  and  narrowing  of  these  vessels,  with  the  result 
that  the  free  passage  of  blood  through  them  may  be  interfered 
with. 


DISEASES   OF   THE   PERICARDIUM         131 


SYMPTOMS  AND   PHYSICAL  SIGNS 

Pericardial  adhesion  is  frequently  unattended  by  symptoms  of 
any  kind.  Moreover,  the  symptoms  that  may  arise  in  connection 
with  this  condition  are  seldom  of  much  diagnostic  value,  inasmuch 
as  their  occurrence  can,  as  a  rule,  be  quite  as  readily  accounted 
for  on  the  ground  of  functional  disturbance  of  the  heart  or  of  some 
other  organic  cardiac  lesion. 

At  the  same  time,  the  appearance  of  such  symptoms  as  prsecordial 
uneasiness  or  pain,  palpitation,  and  dyspnoea  on  very  slight  pro- 
vocation would,  in  the  absence  of  a  more  obvious  cause,  suggest 
the  presence  of  pericardial  adhesion. 

The  symptoms  and  signs  of  failure  of  the  right  ventricle  afford 
valuable  evidence  of  pericardial  adhesion,  provided  the  other  con- 
ditions which  may  give  rise  to  this  event  can  be  excluded,  or  can 
be  shown  to  be  inadequate  for  the  production  of  the  cardiac 
disability. 

Adherent  pericardium  is  occasionally  a  cause  of  rapid  or  even 
sudden  death. 

PHYSICAL  SIGNS 

Although  it  is  frequently  possible  to  recognise  the  existence  of 
pericardial  adhesion  by  means  of  physical  examination,  it  not 
uncommonly  happens  that  signs  are  either  undiscoverable  or  in- 
conclusive. They  are  most  marked  when  the  adhesions  are 
extensive,  dense,  and  external,  as  well  as  internal. 

The  physical  signs  of  pericardial  adhesion  are  variously  combined, 
but  for  descriptive  purposes  they  will  be  considered  in  the  order 
in  which  they  would  come  under  observation  during  a  clinical 
examination  of  the  chest  and  cardio-vascular  system. 

The  Signs  elicited  by  Inspection  and  Palpation. 

1.  In  rare  instances  a  permanent  depression  or  flattening  of  the 
prsecordial  area  is  observed. 

More  commonly,  however,  there  is  bulging  of  this  portion  of  the 
chest  wall  owing  to  enlargement  of  the  heart  from  valvular  disease 
or  other  cause  acting  concurrently  with  the  pericardial  adhesion. 

2.  A  visible  recession  or  retraction  of  the  intercostal  spaces,  ribs, 
cartilages,  or  sternum  in  the  prsecordial  area,  or  of  certain  other 
portions  of  the  chest  wall,  coincident  with  the  systole  of  the 
ventricles,  affords  valuable  evidence  of  the  existence  of  adherent 
pericardium.  Systolic  depression  of  the  intercostal  spaces  in  the 
immediate  neighbourhood  of  the  apex  beat  may  occur  independently 
of  pericardial  adhesion,  but  a  visible  recession  of  the  costal  car- 
tilages, ribs,  or  lower  end  of  the  sternum,  with  the  ventricular 
contraction,  is  almost  conclusive  evidence  of  this  condition. 


132  DISEASES   OF   THE    HEART 

Systolic  retraction  of  the  posterior  or  lateral  portions  of  the 
chest  wall,  along  the  line  of  origin  of  the  diaphragm  from  the 
cartilages  of  the  false  ribs,  is  mentioned  by  Dr.  John  Broadbent 
as  an  important  and  reliable  indication  of  adherent  pericardium. 

Diastolic  collapse  of  the  jugular  veins  at  the  root  of  the  neck, 
with  or  without  systolic  retraction  of  the  soft  parts  in  the  same 
situation,  is  occasionally  observed  in  cases  of  adherent  pericardium, 
but  is  of  little  diagnostic  value. 

3.  The  presence  of  diastolic  retraction  of  the  intercostal  spaces 
in  the  prfecordial  area  is  of  considerable  diagnostic  importance, 
since  it  is  a  sign  that  could  hardly  be  caused  by  anything  but 
pericardial  adhesion. 

4.  Complete  arrest  of  the  slight  respiratory  movements  which  are 
normally  seen  in  the  upper  part  of  the  epigastric  triangle  formed  by 
the  divergence  of  the  costal  cartilages  is,  according  to  Sir  William 
Broadbent,  a  constant  indication  of  the  adhesion  of  the  heart  to  the 
pericardium  and  central  tendon  of  the  diaphragm. 

5.  Fixation  of  the  apex  beat  affords  valuable  evidence  of  peri- 
cardial adhesion.  The  apex  beat,  which  may  or  may  not  be  dis- 
placed, does  not  descend  during  inspiration,  and  the  position  of  the 
cardiac  impulse  is  unaffected  by  change  of  posture. 

6.  On  rare  occasions  a  diastolic  rebound  of  some  portion  of  the 
chest  wall  in  the  prjecordial  area  succeeds  the  systolic  recession  of 
the  ribs  and  sternum  that  was  mentioned  above.  It  can  be  felt  by 
the  hand  as  an  impulse  during  the  diastole  of  the  heart.  The 
presence  of  this  sign  would  per  se  be  sufficient  to  establish  a 
diagnosis  of  adherent  pericardium. 

The  undulatory  movements  which  may  be  seen  in  the  precordial 
area  in  cases  of  pericardial  adhesion  are  of  httle  or  no  diagnostic 
value. 

Duroziez  maintains  the  importance  of  comparing  the  signs 
afforded  by  inspection  and  palpation  in  the  diagnosis  of  adherent 
pericardium,  inasmuch  as  they  are  apparently  contradictory :  for 
during  the  systole  of  the  heart  the  eye  perceives  a  recession  of  the 
chest  wall,  while  the  hand  detects  an  impulse. 


The  Signs  elicited  by  Percussion 

A  permanent  increase  in  the  area  of  the  superficial  cardiac  dulness 
is  frequently  associated  with  the  formation  of  external  pericardial 
adhesions,  by  reason  of  the  attendant  collapse  and  retraction  of  the 
superjacent  pulmonic  tissue,  and  the  consequent  abnormal  exposure 
of  the  heart  and  great  vessels. 

Furthermore,  the  area  of  superficial  cardiac  dulness  may  be 
unaffected  by  inspiration,  owing  to  the  fixing  of  the  anterior  margins 
of  the  lungs  by  the  adhesions. 


DISEASES   OF   THE   PERICARDIUM  133 

These  signs  are,  however,  also  observed  in  connection  with 
inflammatory  conditions  of  the  pleurte,  hence,  unless  supported 
by  other  evidence,  they  are  of  little  value  in  the  diagnosis  of 
adherent  pericardium. 

Evidence  of  enlargement  of  the  right  side  of  the  heart,  in  the 
shape  of  an  increase  of  dulness  to  the  right  of  the  sternum,  is  not 
uncommonly  obtained. 

The  Signs  elicited  by  Auscultation 

Auscultation  does  not  afford  much  assistance  in  the  diagnosis  of 
pericardial  adhesion.  The  sounds  of  the  heart  have  in  some  instances 
a  peculiarly  superficial  character,  and  the  second  sound  at  the  base 
is  very  commonly  reduplicated.  It  cannot  be  said,  however,  that 
either  of  these  signs  is  of  any  real  diagnostic  importance. 

The  Signs  elicited  by  an  Examination  of  the  Pulse 

The  presence  of  adhesions  between  the  pericardium,  chest  wall, 
and  great  vessels  at  the  base  of  the  heart  was  supposed  to  be 
characterized  by  the  pulsus  paradoxus,  a  condition  in  which  the 
pulse  wave  is  diminished  or  lost  during  each  inspiration.  It  was 
thought  that  the  tightening  of  the  adhesions  round  the  aorta, 
produced  by  the  upward  and  outward  movement  of  the  chest  wall 
during  inspiration,  led  to  so  great  a  constriction  of  the  lumen  of 
the  vessel  that  the  heart  was  unable  to  drive  blood  through  it ; 
hence  the  pulse  could  not  reach  the  wrist. 

It  is  improbable  that  the  lumen  of  a  strong-walled  vessel  like  the 
aorta  could  be  constricted  in  the  manner  suggested,  and,  apart  from 
this  difficulty,  it  was  observed  that  the  sign  in  question  was  not  only 
frequently  absent  under  the  conditions  specified,  but  could  be 
detected  with  various  other  lesions  such  as  pericardial  effusion, 
dilatation  of  the  heart,  etc.,  in  which  the  mechanism  of  production, 
as  described  above,  could  not  possibly  obtain.  For  these  reasons 
the  sign  has  been  abandoned  as  a  distinctive  indication  of  the 
presence  of  pericardial  adhesion. 

It  is  probable  that  the  occurrence  of  the  pulsus  paradoxus  depends 
in  all  cases  on  the  inability  of  a  weakened  left  ventricle  to  adequately 
meet  the  additional  work  imposed  on  it  by  the  increased  negative 
tension  which  obtains  in  the  thorax  during  inspiration. 

Consequently,  it  happens  that  during  inspiration  the  force  of  the 
ventricular  contraction  becomes  expended  before  the  pulse  wave 
reaches  the  wrist. 

DIAGNOSIS 

Post-mortem  records  bear  ample  testimony  to  the  difficulties 
presented  by  the  diagnosis  of  adherent  pericardium.  Nevertheless 
it  is  frequently  possible,  by  means  of  a  careful  survey  and  com- 
parison of  the  symptoms  and  physical  signs,  to  recognize  with 
certainty  the  existence  of  pericardial  adhesion  during  life. 

A  history  of  pericarditis,  or  of  cardiac  inflammation  during  child- 


134  DISEASES   OF  THE   HEART 

hood,  would  strongly  suggest  the  presence  of  adhesions,  but  in  a 
large  number  of  instances  no  such  history  is  obtainable. 

The  diagnostic  value  of  the  various  symptoms  and  physical  signs 
which  may  be  observed  in  connection  with  adherent  pericardium 
has  already  been  indicated,  and  it  is  necessary  only  to  add  that 
the  information  derived  from  these  sources  should  be  carefully 
weighed  and  compared. 

At  one  time  the  symptoms,  at  another  the  physical  signs,  supply 
the  evidence  on  which  the  diagnosis  is  based,  while  in  a  third  set 
of  cases  it  is  some  apparent  inconsistency  in  the  relation  between 
the  symptoms  and  signs  that  provides  the  clue  to  the  recognition 
of  the  lesion. 

The  appearance  of  the  symptoms  of  cardiac  failure,  or  the 
presence  of  the  signs  of  enlargement  of  the  heart,  would,  in  the 
absence  of  a  discoverable  or  sufficient  cause,  suggest  the  existence 
of  pericardial  adhesion. 

Furthermore,  should  the  symptoms  associated  with  a  lesion  of 
the  heart  be  more  severe  than  the  attendant  physical  signs  can 
account  for,  or  should  rupture  of  compensation,  in  case  of  valvular 
or  other  cardiac  disease,  take  place  without  sufficient  or  apparent 
cause,  the  presence  of  adherent  pericardium  may  reasonably  be 
suspected. 

The  absence  of  any  response  to  treatment  may  be  due  to  a 
similar  cause. 

It  has  been  pointed  out  by  Sir  Samuel  Wilks  that  the  occurrence 
of  severe  cardiac  symptoms  in  young  people,  without  evidence  of 
valvular  disease,  suggests  the  presence  of  pericardial  adhesions. 

PROGNOSIS 

If  the  pathological  effects  of  pericardial  adhesion  on  the  heart 
are  produced  in  the  manner  previously  described,  it  follows  that 
the  prognosis  of  the  lesion  depends  mainly  on  the  extent  to  which 
the  myocardium  is  implicated  in  the  preliminary  inflammatory 
changes. 

If,  therefore,  after  an  attack  of  pericarditis  the  size  of  the  heart 
remains  unchanged,  or  is  but  slightly  increased,  the  outlook, 
speaking  generally,  is  favourable. 

On  the  other  hand,  the  occurrence  of  great  enlargement  of  the 
heart,  more  especially  in  the  form  of  dilatation,  renders  the 
prognosis  much  more  serious. 

It  is  probable  that  pericardial  adhesions,  unless  very  dense  and 
extensive,  are,  per  se,  of  little  practical  importance. 

Pericardial  adhesion  complicated  by  valvular  disease  seldom 
admits  of  a  favourable  prognosis,  inasmuch  as  the  myocardial 
inflammatory  changes  usually  associated  with  the  former  lesion 
militate  against  the  establishment  and  maintenance  of  compensa- 
tion. 


DISEASES   OF   THE   PERICARDIUM         135 

TREATMENT 

It  is  not  possible  to  remove  the  organic  changes  associated  with 
pericardial  adhesion,  hence  the  object  of  treatment  is  to  minimize 
and  delay,  so  far  as  possible,  their  injurious  effect  on  the  heart. 

The  nutrition  of  the  myocardium  must  be  promoted  and  main- 
tained by  suitable  hygienic,  dietetic,  and  medicinal  means,  and  all 
sources  of  cardiac  strain  should  be  carefully  avoided. 

A  more  detailed  description  of  the  measures  by  which  these 
indications  are  carried  out  will  be  given  under  the  account  of  the 
treatment  of  affections  of  the  myocardium. 

The  treatment  of  cardiac  failure  should  be  conducted  on  general 
principles,  but  care  must  be  observed  in  the  use  of  cardiac  tonics. 


SECTION   III 
HYDROPERICARDIUM 

Dropsy  of  the  pericardium  is  due  either  to  (a)  general  or  (5)  local 
causes. 

Under  the  first  head  the  hydropericardium  is  usually  one  of  the 
phenomena  of  general  dropsy  consequent  on  disease  of  the  heart, 
kidneys,  or  lungs,  but  it  may  appear,  in  common  with  effusion  into 
the  other  large  serous  sacs,  during  the  early  stages  of  acute  Bright's 
disease,  or  in  the  course  of  the  cachexia  associated  with  tuber- 
culosis, cancer,  and  the  graver  forms  of  ansemia,  etc. 

In  rare  instances  hydropericardium  depends  on  a  local  obstruction 
to  the  circulation  through  the  pericardial  and  cardiac  veins  caused  by 
thrombosis  of  these  vessels,  or  by  pressure  upon  them  from  without, 
etc.  Dropsy  of  the  pericardium  is  rarely  large  in  amount.  It  gives 
rise  to  the  signs  which  have  already  been  considered  in  connection 
with  pericarditis  with  effusion. 

Hydropericardium  may,  however,  be  distinguished  from  peri- 
carditis with  effusion  by  (i)  the  history  of  one  or  other  of  the 
conditions  mentioned  above,  (2)  the  absence  of  fever,  (3)  the 
absence  of  friction  signs,  and  (4)  the  presence  of  general  oedema 
and  of  effusion  into  the  other  large  serous  cavities. 

The  treatment  of  hydropericardium  is  that  of  the  primary  disease. 
A  large  effusion  may  necessitate  paracentesis  of  the  pericardium. 

SECTION   IV 

HiEMOPERICARDIUM 

Haemorrhage  into  the  pericardial  cavity  is  usually  due  to  the 
bursting  of  an  aneurism  of  the  first  part  of  the  aorta,  or  of  one 
of  the  coronary  arteries,  or  to  rupture  of  the  wall  of  the  heart,  the 
result  of  traumatism,  or  disease  of  the  myocardium. 


136  DISEASES   OF   THE    HEART 

It  may  also  occur,  to  a  much  slighter  extent,  in  pericarditis  due  to 
tubercle,  cancer,  or  scurvy,  and  it  occasionally  depends  on  the 
rupture  of  recent  pericardial  adhesions. 

The  clinical  phenomena  associated  with  this  condition  depend, 
to  some  extent,  on  the  rapidity  of  the  bleeding  into  the  pericardial 
sac.  If  the  haemorrhage  takes  place  gradually,  prsecordial  pain, 
urgent  dyspnoea,  syncopal  attacks,  collapse,  and  evidence  of  loss  of 
blood  may  usher  in  the  fatal  termination.  A  physical  examination 
of  the  chest,  when  it  can  be  made,  discovers  the  signs  of  fluid  in 
the  pericardial  cavity.  The  sudden  discharge  of  a  large  quantity  of 
blood  into  the  pericardial  sac  usually  leads  to  sudden  death. 

Treatment  can  be  palliative  only. 

SECTION    V 
PNEUMOPERICARDIUM 

Pneumopericardium,  as  a  clinical  phenomenon,  is  an  exceedingly 
rare  condition. 

The  means  by  which  air  or  gas  gains  access  to  the  pericardial  sac 
is  either  a  wound  of  the  thorax  involving  the  parietal  layer  of  the 
pericardium,  or  the  establishment  of  a  communication  between 
the  pericardium  and  an  air  or  gas-containing  organ,  such  as  the 
oesophagus,  lungs,  or  pleurae,  stomach  or  intestines.  In  the  second 
and  more  common  event  the  extension  to  the  pericardium  of 
suppurative  or  ulcerative  processes  affecting  one  or  other  of  these 
viscera  is  the  determining  cause  of  the  perforation  of  the  membrane. 

Pericarditis  quickly  follows  the  entrance  of  air  or  gas  into  the 
pericardial  cavity,  and  since  the  effusion  which  accompanies  the 
inflammatory  process  is  almost  invariably  purulent,  a  condition  of 
pyopneumopericardium,  rarely  of  hydropneumopericardium  is 
produced. 

The  spontaneous  development  of  gas  in  the  pericardial  cavity, 
consequent  on  the  presence  of  gas  forming  bacilli,  is  postulated  by 
some  observers. 

The  symptoms  associated  with  pneumopericardium  are  practically 
those  of  purulent  pericarditis. 

The  physical  signs  are  often  very  remarkable  and  are  characteristic 
of  the  presence  of  gas  and  fluid  together  in  the  pericardial  sac. 

Bulging  of  the  praecordial  area  is  sometimes  very  pronounced. 
The  hand  placed  over  the  heart  occasionally  experiences  a  succession 
of  small  shocks  or  vibrations  due  to  the  bursting  of  air  bubbles 
at  the  surface  of  the  fluid.  In  the  recumbent  posture  a  clear 
tympanitic  percussion  note  is  obtained  over  the  cardiac  area,  and 
when  the  opening  into  the  pericardial  sac  is  patent,  a  cracked 
pot  sound  may  be  elicited. 

If  the  patient  is  made  to  sit  up  and  lean  forwards,  the  tympanitic 
note  is  replaced  over  the  lower  portion  of  the  prgecordial  area 
by  a  dull  sound,  in  consequence  of  the  displacement  of  the  gas 
by  fluid,  under  the  influence  of  gravity. 


DISEASES   OF   THE   PERICARDIUM         137 

For  a  similar  reason  a  partial  replacement  of  the  lateral  extent  of 
the  area  of  resonance  by  dulness  can  be  effected  by  turning  the 
patient  to  one  side  or  the  other. 

The  sounds  of  the  heart  have  a  characteristic  metallic  quality,  and 
are  described  as  splashing,  gurghng,  churning,  etc.  They  have  also 
been  compared  to  the  sound  produced  by  a  water-wheel  in  motion. 

An  amphoric  echo  of  the  heart  sounds,  and  of  pericardial  friction 
sound,  etc.,  has  been  observed  in  some  instances. 

In  the  presence  of  the  physical  signs  just  mentioned  the  diagnosis 
of  pneumopericardium  presents  no  difficulty.  The  prognosis  is  very 
unfavourable,  but  recovery  has  been  recorded  in  cases  due  to  injury. 

There  is  little  scope  for  treatment,  which  should  be  conducted  on 
the  lines  indicated  under  the  head  of  ^'  Acute  Pericarditis." 

The  question  of  operative  procedure,  in  the  shape  of  paracentesis 
pericardii,  or  of  free  drainage  of  the  pericardial  sac,  has  to  be  taken 
into  consideration  in  every  case. 

SECTION   VI 
NEW  GROWTHS 

The  more  important  new  growths  which  may  affect  the  pericardium 
are  tubercle,  carcinoma,  and  sarcoma. 

Tubercular  disease  of  the  pericardium  is  uncommon,  and  its 
occurrence  is  usually  secondary  to  tubercular  disease  elsewhere. 

A  primary  form  of  pericardial  tuberculosis  associated  only  with 
caseation  of  the  bronchial  or  anterior  mediastinal  glands  is  described 
by  Osier. 

In  a  large  number  of  instances  the  implication  of  the  pericardium 
is  due  to  the  direct  extension  of  tubercular  disease  from  the  lungs. 
The  pericardium  is  very  rarely  affected  in  cases  of  general  acute 
miliary  tuberculosis. 

Carcinoma  of  the  pericardium  is  very  rare  and  always  secondary. 
The  pericardium  usually  becomes  involved  by  the  direct  extension 
of  the  growth  from  neighbouring  structures. 

The  sarcomata  are  nearly  always  secondary,  and  are  of  the  spindle 
or  round  cell  variety. 

Lymphosarcomata  commonly  originate  in  the  mediastinal  tissue 
and  attack  the  parietal  layer  of  the  pericardium  almost  exclusively. 

Syphilitic  affections  of  the  pericardium  are  almost  invariably 
secondary  to  lesions  of  the  myocardium.  New  growths  of  the 
pericardium  usually  give  rise  to  chronic  inflammation  of  the  mem- 
brane, attended,  in  many  instances,  by  effusion  of  blood  or  pus. 

Clinically,  the  implication  of  the  pericardium  in  a  new  growth 
may  be  suspected  when  the  symptoms  and  signs  of  pericarditis  are 
observed  in  conjunction  with  tubercular  disease  of  the  lungs  or 
other  organs,  or  with  an  intra-thoracic  tumour. 

The  prognosis  is,  of  course,  hopeless,  and  treatment  can  be 
palliative  only. 


CHAPTER   VIII 
ACUTE   ENDOCARDITIS 


Classification — Section  I.  Acute  Simple  Endocarditis — Section  II.  Malignant  or 

Infective  Endocarditis. 

Inflammation  of  the  endocardium  may  be  either  acute  or  chronic, 
and  in  the  large  majority  of  cases  the  morbid  process  is  Hmited  to 
the  valves  of  the  heart  and  their  tendinous  attachments. 

It  is  customary  to  distinguish  two  kinds  of  acute  endocarditis, 
viz. : — 

1.  Acute  simple  endocarditis 

2.  Acute  malignant  or  infective  endocarditis 

This  division  of  the  subject  is  not  altogether  satisfactory,  either 
from  a  clinical  or  pathological  point  of  view,  but  it  is  the  most 
suitable  for  descriptive  purposes,  and  will  therefore  be  adopted. 


SECTION    I 

ACUTE   SIMPLE  ENDOCARDITIS 

iETIOLOGY 

Acute  simple  endocarditis  arises  most  commonly  in  the  course  of  an 
attack  of  acute  or  sub-acute  rheumatism,  and  may  precede,  accompany, 
or  follow  the  aifection  of  the  joints.  It  occurs  in  about  50  per  cent, 
of  the  cases  of  acute  rheumatism,  and  the  liabiHty  of  the  endo- 
cardium to  be  affected  increases  with  repeated  attacks  of  rheumatic 
fever. 

Endocarditis  of  rheumatic  origin  occurs  more  frequently  in  children 
than  in  adults,  and  the  vulnerability  of  the  endocardium  appears  to 
be  most  marked  between  the  ages  of  four  and  twelve.  The  large 
majority  of  the  cases  of  rheumatic  endocarditis  occur  in  persons 
under  thirty  years  of  age,  and  women  suffer  rather  more  frequently 
than  men. 

138 


ACUTE   ENDOCARDITIS  139 

There  is  no  relation  between  the  occurrence  of  endocardial  in- 
flammation in  acute  rheumatism  and  the  amount  of  pyrexia,  or  the 
severity  of  the  joint  implication. 

The  endocarditis  which  arises  in  the  course  of  a  considerable 
number  of  cases  of  chorea  is,  probably,  of  rheumatic  origin. 

Acute  endocarditis  is  also  observed  in  connection  with  the  acute 
zymotic  fevers,  more  especially  with  scarlet  fever  and  measles.  It 
occasionally  arises  in  association  with  enteric  fever,  variola,  diph- 
theria, and  with  other  septic  conditions,  such  as  erysipelas,  puerperal 
fever,  septicaemia,  and  pyaemia. 

In  some  instances  it  has  occurred  as  a  complication  of  pneumonia, 
syphilis,  and  gonorrhoea. 

Among  other  occasional  causes  of  endocarditis  may  be  mentioned 
such  disorders  as  gout,  acute  nephritis,  and  diabetes. 

Acute  and  chronic  tuberculosis  are  sometimes  accompanied  by 
endocardial  inflammation,  and  in  a  few  instances  the  tubercle 
bacillus  has  been  demonstrated  in  the  affected  parts. 

Several  cases  have  been  recorded  in  which  endocarditis  has 
followed  a  blow  on  the  chest.  Here  the  endocardial  inflammation 
depends  in  all  probability  on  the  rupture  or  tearing  of  a  valve. 

The  occurrence  of  acute  simple  endocarditis  as  a  primary  or 
idiopathic  affection  is  mentioned  by  some  observers,  but  it  must 
be  an  exceedingly  rare  event.  The  exclusion  of  a  rheumatic 
origin  must  be  very  difficult  in  cases  of  this  kind,  since  it  is 
probable  that  endocarditis  is,  in  some  instances,  the  sole  expression 
of  the  rheumatic  state.  The  presence  of  old -standing  valvular 
disease,  the  result  of  acute  or  chronic  inflammation,  or  of  de- 
generative changes,  is  a  powerful  predisposing  cause  of  acute 
endocarditis. 

Endocarditis  may  be  hereditary  in  so  far  as  the  diseases  with 
which  it  is  associated  are  hereditary.  Unhealthy  hygienic  sur- 
roundings, poverty,  and  exposure  are  of  influence  in  the  causation 
of  endocardial  disease,  by  reason  of  the  fact  that  such  conditions 
predispose  to  rheumatism  and  other  disorders  which  may  give  rise 
to  endocarditis. 

PATHOLOGY  AND   MORBID  ANATOMY 

The  inflammatory  changes  in  acute  endocarditis  are  usually 
limited  to  the  valves  of  the  heart  and  their  tendinous  attachments, 
by  reason  of  the  greater  strain  to  which  these  structures  are  sub- 
jected as  compared  with  the  rest  of  the  endocardium. 

Furthermore,  the  morbid  process  in  adults  is  almost  invariably 
confined  to  the  valvular  apparatus  of  the  left  heart.  This  is 
accounted  for  on  the  grounds  that  the  endocardium  is  rendered 
more  vulnerable  by  the  higher  blood  pressure  and  greater  varia- 
tion of  intra-cardic  tension  which  obtain  on  this  side  of  the 
organ.     For  a  similar  reason  foetal  endocarditis  most  commonly 


HO  DISEASES    OF   THE    HEART 

affects  the  right  side  of  the  heart.  Acute  endocarditis  of  the  tricuspid 
valve  does,  however,  occur  in  adults,  and  Byrom  Bramwell  considers 
that  it  is  more  common  than  is  generally  supposed.  The  pulmonic 
valve  is  very  rarely  affected. 

The  mitral  valve  is  more  frequently  the  seat  of  acute  rheumatic 
endocarditis  than  the  aortic,  owing,  it  is  supposed,  to  the  fact  that, 
under  normal  conditions,  the  mitral  curtains  are  subjected  to 
greater  pressure  and  stress  during  the  closing  of  the  orifice  than 
is  the  case  with  the  aortic  cusps.  It  is  instructive  to  note  in  this 
connection  the  more  common  implication  of  the  aortic  valve  in 
persons  who  are  engaged  in  laborious  occupations ;  that  is,  under 
conditions  which  expose  the  valve  to  strain. 

The  earliest  and  most  intense  inflammatory  changes  are  observed 
in  those  portions  of  the  valve  which  are  most  exposed  to  friction 
and  pressure.  These  conditions  are  determined  by  the  direction 
of  the  blood  stream  and  by  the  lines  of  maximum  contact  of  the 
opposed  valvular  segments.  Consequently  the  auricular  surface  of 
the  mitral  and  tricuspid,  and  the  ventricular  surface  of  the  semilunar 
valves,  just  within  the  free  margin  of  each  flap,  are  the  parts  chiefly 
affected. 

The  chordae  tendineae  are  frequently  implicated  in  the  morbid 
process,  and  sometimes  the  general  lining  of  the  heart  (mural 
endocarditis),  especially  in  the  neighbourhood  of  the  valves,  is 
attacked. 

The  earliest  manifestation  of  acute  endocarditis  visible  to  the 
naked  eye  is  a  milky  opacity  of  the  endocardium,  accompanied  by 
the  development  of  small  translucent  nodulated  swelHngs,  which  re- 
semble a  string  of  fine  beads,  arranged  just  within  the  free  margins 
of  the  affected  valve  segments. 

These  projections,  which  are  the  result  of  the  accumulation  in 
the  sub-endothelial  tissues  of  inflammatory  products,  subsequently 
increase  in  size,  in  consequence  of  the  deposition  upon  them  of 
a  varying  quantity  of  fibrin  from  the  blood.  The  outgrowths, 
thus  formed,  are  known  as  vegetations.  Similar  appearances  may 
be  observed  in  the  endocardium  covering  the  chordae  tendineae, 
or  other  parts  of  the  internal  surface  of  the  heart. 

The  vegetations  are  usually  sessile,  less  commonly  pedunculated, 
and  they  vary  greatly  in  size,  in  accordance  with  the  stage,  extent, 
and  severity  of  the  inflammatory  process  and  the  amount  of  the 
fibrinous  deposit. 

Before  describing  the  microscopical  appearances  in  acute  endo- 
carditis, a  brief  reference  must  be  made  to  the  normal  histological 
structure  of  the  endocardium.  The  membrane  consists  internally 
of  a  single  layer  of  flat  polygonal  endothelial  cells,  resting  on 
a  thin  elastic  lamina,  which  is  supported  by  a  stratum  of  nucleated 
branched  connective  tissue  cells,  containing  a  dense  network  of 
fine  elastic  fibres.  Outside  this  is  a  layer  of  coarse  fibro-elastic  tissue, 
arranged   in   the   form   of   trabeculae,   which   becomes   continuous 


ACUTE  ENDOCARDITIS  141 

with  the  sub-endocardial  connective  tissue,  and  through  this  with 
the  intermuscular  connective  tissue.  The  blood  vessels  supplying 
the  endocardium  are  situated  in  the  sub-endocardial  connective 
tissue. 

They  accompany  the  muscular  fibres  and  are  not  found  elsewhere. 

The  flaps  of  the  cardiac  valves  are  made  up  of  folds  of  the  endo- 
cardium, separated  and  held  together  by  fine  fibro-elastic  tissue. 

In  adults  the  auriculo-ventricular  curtains  contain  striped  mus- 
cular fibres  in  the  inner  thirds  of  their  radial  extent,  which  are 
continuous  with  the  muscle  of  the  auricular  wall.  The  semilunar 
cusps  are  devoid  of  muscular  tissue.  It  follows  from  what  has 
already  been  said  with  regard  to  the  blood  supply  of  the  endo- 
cardium, that  the  semilunar  cusps,  and  the  outer  two-thirds  of  the 
auriculo-ventricular  segments,  are  destitute  of  blood  vessels,  though 
they  contain  a  rich  network  of  lymphatics. 

Under  the  microscope,  the  most  striking  feature  of  the  morbid 
process,  in  the  early  stages  of  acute  endocarditis,  is  seen  to  be  a 
general  infiltration  of  the  structure  of  the  valve  with  small  round  cells. 
They  are  mainly  derived  from  the  proliferation  of  the  connective 
tissue  corpuscles,  situated  immediately  beneath  the  endothelium, 
though  to  some  extent,  no  doubt,  they  are  the  result  of  a  leucocytic 
infiltration  of  the  inflamed  part.  In  other  portions  of  the  endo- 
cardium the  increase  of  the  cellular  elements  is  always  most  marked 
in  the  sub-endothelial  connective  tissue  layer.  The  deeper  layers 
of  the  membrane  and  the  adjacent  intermuscular  septa  are  also 
affected,  but  in  a  less  degree. 

As  the  inflammatory  process  progresses  the  outline  of  the  white 
fibres  becomes  indistinct,  and  is  finally  lost,  so  that  the  cells  appear 
to  lie  in  a  homogeneous  matrix.  This  phenomenon  is  exceptionally 
well  seen  in  the  course  of  the  valvular  inflammation,  and  is  appar- 
ently due  to  the  gradual  absorption  of  the  white  fibres. 

The  cellular  elements  are  not  evenly  distributed  throughout  the 
valve,  but  are  aggregated  at  certain  points,  i.e.  just  inside  the  free 
edges  of  the  cusps,  and  correspond  with  the  small  projections  pre- 
viously mentioned.  The  endothelium  in  these  situations  becomes 
stretched,  undergoes  granular  degeneration,  and  finally  desquamates, 
and  the  underlying  elastic  lamina  also  breaks  up. 

The  small  cell-capped  projections  are  thus  brought  into  direct 
contact  with  the  blood  stream,  and  fibrin  is  deposited  upon  them 
in  the  form  of  fibrillar  or  wavy  granular  masses,  inclosing  leucocytes, 
and  in  some  instances  certain  micro-organisms,  to  wit,  staphylococci, 
streptococci,  or  diplococci. 

The  vegetations  formed  in  this  way  continue  to  increase  in  size 
owing  to  the  further  deposition  of  fibrin  upon  them,  and  they 
frequently  acquire  a  villous  or  branched  appearance  by  the  forma- 
tion of  secondary  outgrowths  from  their  free  extremities. 

It  will  be  observed  that  the  vegetations  are,  at  first,  without  blood 
vessels. 


142  DISEASES   OF   THE    HEART 

The  subsequent  changes  consist  in  the  gradual  absorption  and 
cicatrization  of  the  inflammatory  products,  and  during  this  process 
the  vegetations  become  vascularized  by  the  ingrowth  of  new  vessels 
from  the  base  of  the  valve. 

The  ultimate  effects  of  an  acute  inflammation  of  the  endocardium 
on  the  valves  of  the  heart  are  numerous,  and  they  vary  considerably 
in  different  cases. 

It  is  said  that  in  its  early  stages  the  inflammatory  exudation  may 
be  completely  absorbed  without  producing  any  permanent  alteration 
in  the  structure  of  the  affected  valve,  but  such  a  result  must  be 
exceedingly  rare. 

In  the  large  majority  of  cases  the  process  of  healing  is  accom- 
panied by  fibrous  thickening,  and  induration  of  the  orifices  and 
curtains  of  the  valves. 

The  subsequent  contraction  of  the  newly  formed  tissue  may  give 
rise  either  to  the  narrowing  of  an  orifice,  or  to  the  puckering  and 
distortion  of  the  segments  of  a  valve,  and  thereby  to  its  incom- 
petence, or,  as  most  commonly  happens,  to  a  combination  of  these 
two  conditions. 

The  curtains  of  a  valve  sometimes  become  adherent  to  one 
another,  or  to  the  wall  of  the  heart,  with  the  production,  in  the 
first  event,  of  valvular  obstruction,  and,  in  the  second,  of  valvular 
incompetence. 

The  vegetations  not  uncommonly  undergo  ulcerative  changes, 
which  may  lead  to  aneurism,  perforation,  or  rupture  of  the  cusps  of 
a  valve. 

Rupture  of  the  chordae  tendineae  is  occasionally  produced  in  this 
way,  and  it  not  infrequently  happens  that  the  efficient  action  of 
these  structures  is  impaired  by  implication  of  the  musculi  papillares 
in  the  infiammatory  process. 

Large  vegetations  may  mechanically  interfere  with  the  closure  of 
a  valve,  or  may  obstruct  the  blood  flow  through  its  orifice. 

Portions  of  the  vegetations  sometimes  become  detached  and  swept 
into  the  blood  stream,  and  in  this  way  give  rise  to  embolism  in 
distant  organs,  such  as  the  brain,  spleen,  kidneys,  etc. 

The  thickened  endocardium  is  liable,  in  course  of  time,  to  under- 
go atheromatous  changes,  which  may  be  accompanied  by  ulceration 
or  calcification  of  the  affected  tissues  (see  "  Chronic  Endocarditis," 
pp.   i6o). 

Extension  of  the  inflammatory  process  from  the  cardiac  valves  to 
the  wall  of  the  heart  is  not  uncommon,  and  is  followed  by  more  or 
less  intermuscular  fibrosis  and  induration  of  the  myocardium.  The 
muscle  fibres  may  undergo  degenerative  changes,  due  either  to 
myocarditis  or  to  compression. 

Inflammation  afi'ecting  the  aortic  valve  occasionally  spreads  to  the 
wall  of  the  aorta,  and  may  give  rise  to  weakening  and  dilatation  of 
the  root  of  this  vessel. 

The  secondary  effects  of  endocarditis  are  the  production  of  hyper- 


ACUTE   ENDOCARDITIS  143 

trophy  and  dilatation  of  the  heart,  together  with  the  changes  to 
which  these  conditions  are  liable  to  give  rise. 

Endocarditis  is  frequently  complicated  by  pericarditis  or  myo- 
carditis, and  occasionally  by  both  these  affections ;  hence  the  morbid 
appearances  characteristic  of  one  or  other  of  these  diseases  may  also 
be  observed. 

SYMPTOMS 

The  onset  of  acute  endocarditis  is  usually  insidious,  and  in  the 
absence  of  complications  {i.e.  of  myocarditis  or  pericarditis)  is 
seldom  accompanied  by  any  symptoms  that  would  draw  attention  to 
the  heart.  Moreover,  the  symptoms  which  may  arise  in  connection 
with  an  acute  inflammation  of  the  endocardium  are,  as  a  rule,  over- 
shadowed by  those  of  the  disease  with  which  the  endocarditis  is 
associated. 

In  some  instances  the  onset  of  the  affection  is  apparently  shown  by 
an  exacerbation  of  the  pre-existent  febrile  phenomena,  by  praecordial 
uneasiness  or  pain,  palpitation,  dyspnoea,  and  increased  rapidity  of 
the  pulse.  It  is  probable,  however,  that  the  occurrence  of  these 
symptoms  in  the  course  of  acute  endocarditis  is  due  either  to  the  ex- 
tension of  the  inflammatory  process  to  the  wall  of  the  heart,  or  to  the 
incidence  of  pericarditis  or  of  myocarditis.  It  occasionally  happens 
that  symptoms  indicative  of  embolism  are  the  earliest  manifestation 
of  acute  endocarditis.  More  rarely  still,  the  first  indication  of 
inflammation  of  the  endocardium  is  the  appearance  of  the  symptoms 
and  signs  of  embarrassment  of  the  pulmonic  or  systemic  circulation. 
Under  these  circumstances,  however,  the  endocarditis  is  complicated 
by  myo-  or  pericarditis,  or  by  pre-existent  endocardial  disease. 

The  symptoms  of  acute  or  sub-acute  endocarditis  in  children  are 
even  more  obscure  than  in  adults,  and  unless  great  watchfulness  is 
observed  the  occurrence  of  the  disease  in  early  life  may  be  entirely 
overlooked.  The  presence  during  childhood  of  any  of  the  dis- 
orders which  may  be  complicated  by  endocarditis,  and  especially 
the  occurrence  of  any  of  the  manifestations  of  the  rheumatic  state 
— such  as  arthritis,  sub-cutaneous  nodules,  erythema,  tonsillitis,  etc., 
call  for  careful  and  repeated  examinations  of  the  heart. 

PHYSICAL  SIGNS 

The  presence  of  acute  endocarditis  can  sometimes  be  recognised 
with  certainty  by  means  of  a  physical  examination  of  the  heart,  but 
it  not  infrequently  happens  that  the  evidence  afforded  by  this 
method  of  investigation  is  far  from  conclusive.  The  information 
supplied  by  inspection,  palpation,  and  percussion  is  seldom  of  any 
diagnostic  value. 

The  most  rehable  signs  of  acute  simple  endocarditis  are  elicited 
by  means  of  auscultation,  and  consist  in  an  alteration  in  the 
character  of  the  sounds  of  the  heart,  or  in  the  presence  of  a  cardiac 
bruit. 


144  DISEASES   OF  THE    HEART 

The  earliest  and  most  common  modification  of  the  normal 
auscultatory  phenomena  is  a  prolongation  and  muffling  of  the  first 
sound  of  the  heart.  This  is  most  distinctly  heard  at  the  apex,  and  is 
in  all  probability  due  to  impairment  of  the  valvular  element  of 
the  first  sound  by  reason  of  the  swollen  condition  of  the  segments 
of  the  mitral  valve,  which  is  most  frequently  the  seat  of  the  inflam- 
matory process. 

Prolongation  of  the  first  sound  becomes  audible,  as  a  rule,  during 
the  first  few  days  of  the  rheumatic  attack,  and  may  persist  until 
convalescence  is  established,  or  it  may  gradually  develop  into  an 
apical  systolic  murmur.  The  bruit  usually  possesses  a  soft  blowing 
character,  and  is  conveyed  outwards  into  the  axilla,  and  backwards 
as  far  as  the  angle  of  the  left  scapula.  It  indicates  insufficiency  of 
the  mitral  valve. 

The  appearance  of  an  apical  systolic  murmur  during  the  course  of 
acute  rheumatism  may  depend  also  on  muscular  incompetence  of 
the  mitral  valve,  due  either  to  rheumatic  myocarditis,  or  to  muscular 
weakness  consequent  on  the  pyrexia,  or  the  accompanying  anaemia. 
The  clinical  differentiation  of  the  cause  of  the  murmur  will  be  con- 
sidered under  the  head  of  "  Diagnosis." 

A  systolic  murmur  audible  in  the  aortic  area  may  be  due  either 
to  a  valvulitis,  or  to  anaemia;  in  the  pulmonic  area  it  is  almost 
invariably  the  result  of  anaemia. 

A  systolic  murmur  in  the  tricuspid  area  would,  in  the  absence 
of  evidence  of  previous  disease  of  the  heart,  have  the  same  signifi- 
cance with  regard  to  the  condition  of  the  tricuspid  valve  as  an 
apical  systolic  murmur  has  in  respect  to  the  mitral  valve. 

The  presence  of  a  diastolic  or  presystolic  murmur,  which  is,  how- 
ever, not  commonly  heard  at  this  stage  of  the  endocardial  inflam- 
mation, is  conclusive  evidence  of  valvular  disease  of  the  heart. 

Reduplication  of  the  first  or  second  sound  of  the  heart  is  some- 
times observed  as  an  early  indication  of  acute  endocarditis. 

Reduplication  of  the  second  sound  is  occasionally  audible  at  the 
apex  and  not  at  the  base  of  the  heart,  and  the  second  element  of 
the  reduplicated  sound  may  be  foUowed  by  a  soft  diastolic  murmur. 
This  form  of  reduplication  has  been  insisted  upon  by  Cheadle  as 
an  important  sign  of  endocarditis,  and  he  regards  it  as  the  earliest 
indication  of  commencing  obstruction  at  the  mitral  opening. 

The  manner  in  which  reduplication  of  the  sounds  of  the  heart 
is  brought  about  has  been  considered  elsewhere  (see  pp.  51,  52). 

COMPLICATIONS 

It  has  already  been  pointed  out  that  acute  simple  endocarditis 
is  commonly  associated  with  a  variable,  though  usually  slight  degree 
of  myocarditis.  An  extensive  lesion  of  the  myocardium  may  be 
followed  by  acute  dilatation  of  the  heart. 

Pericarditis  complicates  fully  a  third  of  the  cases  of  acute  endo- 


ACUTE   ENDOCARDITIS  145 

carditis.  It  sometimes  precedes,  but  more  often  arises  simultaneous!) 
with,  or  follows  the  endocardial  affection. 

Rupture  of  the  cusp  of  a  valve,  or  of  some  of  the  chordae  ten- 
dinese,  is  an  occasional  complication  of  acute  simple  endocarditis. 

Acute  aortitis,  due  to  the  extension  of  inflammation  from  the 
aortic  valve,  is  of  very  rare  occurrence. 

Embolism  and  haemorrhagic  infarction  of  the  brain,  spleen,  kidneys, 
and  myocardium,  etc.,  may  occur  at  any  stage  of  the  endocardial 
inflammation,  in  consequence  of  the  detachment  of  portions  of  the 
vegetations,  or  of  thrombi,  formed  in  the  auricular  cavities. 

Pulmonary  congestion,  pleurisy,  and  pneumonia  are  sometimes 
observed  in  association  with  acute  endocarditis,  more  especially  with 
extensive  lesions  of  the  mitral  valve. 


COURSE  AND  TERMINATIONS 

The  duration  and  course  of  acute  simple  endocarditis  are  most 
uncertain.  In  a  very  small  proportion  of  the  cases  the  inflammatory 
process  clears  up  without  giving  rise  to  any  permanent  alteration  in 
the  structure  of  the  affected  valve.  It  is  possible,  too,  that  in  a  few 
instances  the  organic  changes  occasioned  in  the  valvular  segments 
are  insufficient  to  interfere  with  the  functional  efficiency  of  the 
valve. 

In  the  large  majority  of  cases,  however,  acute  simple  endocarditis 
leads,  sooner  or  later,  to  chronic  valvular  disease. 

Death,  when  it  takes  place  during  the  acute  stage  of  simple 
endocarditis,  is  usually  due  to  the  occurrence  of  some  complication, 
such  as  acute  dilatation  of  the  heart,  pericarditis  with  effusion, 
embolism,  pneumonia,  etc. 

DIAGNOSIS 

The  diagnosis  of  acute  simple  endocarditis  rests,  for  the  most  part, 
on  the  data  afforded  by  a  physical  examination  of  the  heart.  The 
evidence  derived  from  this  source  is,  however,  not  uncommonly 
equivocal,  so  that  the  recognition  of  the  occurrence  of  the  lesion, 
although  at  times  quite  easy,  is  frequently  difficult,  and  occasionally 
impossible.  In  the  absence  of  a  murmur  over  the  prsecordial  area, 
the  occurrence  of  acute  endocarditis  can  be  suspected  only  when,  in 
the  course  of  acute  rheumatism  or  other  predisposing  cause,  the 
symptoms  of  cardiac  excitement  or  irritation  make  their  appearance, 
and  at  the  same  time  the  first  sound  of  the  heart  is  observed  to 
become  prolonged. 

If  a  murmur  is  heard  over  the  cardiac  region,  it  may  be  produced 
either  inside  or  outside  the  heart. 

The  means  of  distinguishing  between  an  endocardial  and  exo- 
cardial  murmur  have  already  been  indicated  (see  pp.  70,  71). 

L 


146  DISEASES   OF  THE    HEART 

If  the  presence  of  an  endocardial  murmur  can  be  established, 
the  differential  diagnosis  of  its  cause  still  remains  to  be  considered. 
It  has  already  been  pointed  out  that  an  apical  systolic  murmur, 
indicative  of  mitral  regurgitation,  may  be  due  either  to  inflamma- 
tion of  the  valvular  segments,  or  to  muscular  incompetence  of  the 
valve,  consequent  on  myocarditis,  pyrexia,  or  anaemia. 

The  stage  of  the  primary  disease  at  which  the  murmur  is  first 
observed  furnishes  the  most  important  evidence  in  the  discrimina- 
tion of  its  cause.  In  rheumatic  fever  the  apical  murmur  becomes 
audible,  as  a  rule,  during  the  first  few  days  of  the  attack,  whereas 
in  other  febrile  disorders,  such  as  enteric  fever,  etc.,  the  bruit 
appears  in  the  later  stages  of  the  disease. 

In  all  probability,  therefore,  the  source  of  the  murmur  in  the  two 
cases  is  different ;  hence  pyrexia  can  be  excluded  as  the  cause  of 
the  apical  systolic  bruit  which  appears  during  the  early  stages  of 
acute  rheumatism.  Anaemia  can  be  eliminated  on  similar  grounds, 
since  this  condition  does  not  usually  develop  until  the  later  stages 
of  rheumatic  fever.  Moreover,  an  apical  systolic  murmur  of  haemic 
origin  would  be  preceded  and  accompanied  by  a  venous  hum  in  the 
neck  and  a  pulmonary  systolic  bruit,  and  these  are  rarely  observed 
during  the  early  stages  of  rheumatic  fever,  though  they  may  develop 
later. 

The  occurrence  of  acute  rheumatism  in  an  antemic  subject 
would  render  the  differential  diagnosis  of  an  apical  systolic  murmur 
extremely  difficult,  if  not  impossible. 

It  would  appear,  therefore,  that  an  apical  systolic  bruit  audible 
during  the  first  few  days  of  rheumatic  fever  is  in  all  probability  due 
either  to  endocarditis  or  myocarditis,  or  to  a  combination  of  these 
conditions.  Clinically  it  is  difficult,  indeed  well-nigh  impossible,  to 
decide  which  of  these  morbid  processes  has  given  rise  to  the 
valvular  incompetence.  The  disappearance  of  the  murmur  has 
been  held  to  exclude  endocarditis,  but  it  is  possible  that  the  final 
changes  in  the  valve  segments  produced  by  a  valvulitis  might  fall 
short  of  the  amount  necessary  to  give  rise  to  valvular  incompetence. 

The  appearance  of  such  symptoms  as  dyspnoea,  vertigo,  delirium, 
etc.,  in  association  with  a  small,  rapid,  irregular  pulse  and  the  signs 
of  cardiac  dilatation,  would  point  to  the  occurrence  of  myocarditis, 
but  would  not  exclude  endocarditis. 

Valvular  incompetence  of  rheumatic  origin  is  much  more  com- 
monly due  to  endocarditis  than  to  myocarditis,  hence  the  occur- 
rence of  the  former  lesion  is  always  more  probable  than  the  latter. 
Nevertheless,  whether  operative  or  not,  a  greater  or  less  degree  of 
myocarditis  is  frequently  associated  with  acute  inflammation  of  the 
endocardium. 

A  systoHc  murmur  audible  in  the  aortic  area  may  be  due  (so  far 
as  the  present  argument  is  concerned)  either  to  inflammation  of  the 
aortic  valve,  or  to  ancemia.  The  differential  diagnosis  depends  on 
the  period  of  the  rheumatic  attack  at  which  the  bruit  appears,  and 


ACUTE   ENDOCARDITIS  147 

on  the  presence  or  absence  of  other  signs  and  symptoms  of 
anaemia. 

Apart  from  congenital  causes,  a  systolic  murmur  in  the  pulmonic 
area  is  almost  invariably  functional.  The  determination  of  the 
cause  of  the  tricuspid  regurgitant  murmur,  appearing  in  the  course 
of  acute  rheumatism,  depends  on  considerations  similar  to  those 
which  have  already  been  discussed  with  reference  to  the  mitral 
valve. 

A  presystolic  or  diastolic  bruit  is  always  due  to  organic  lesions  of 
the  orifices  or  segments  of  the  valves. 

Accentuation  of  the  pulmonic  second  sound,  if  at  all  marked, 
points  to  organic  disease,  probably  of  the  mitral  valve. 

Signs  of  enlargement  of  either  side  of  the  heart,  or  a  history 
of  dyspnoea,  dropsy,  or  of  a  former  attack  of  rheumatism  is  indica- 
tive of  pre-existent  cardiac  disease.  The  presence  of  an  old  valvular 
lesion,  however,  renders  a  fresh  inflammation  of  the  endocardium 
more  likely,  and  its  occurrence  would  tend  to  aggravate  the  existing 
cardiac  signs  and  symptoms. 

The  differential  diagnosis  of  acute  simple,  and  malignant  endo- 
carditis will  be  considered  under  the  account  of  the  latter  affection. 


PROGNOSIS 

In  attempting  to  forecast  the  issue  of  acute  endocarditis,  the  first 
point  to  be  taken  into  consideration  is  the  severity  of  the  disease 
with  which  the  endocardial  inflammation  is  associated.  Thus  acute 
rheumatism,  chorea,  the  infective  fevers,  etc.,  may  each  give  rise  to 
symptoms  that  are  attended  with  danger  to  life. 

In  the  absence  of  pre-existent  cardiac  disease  the  prognosis  of 
rheumatic  endocarditis  is  favourable  so  far  as  the  immediate  result 
of  the  lesion  is  concerned,  but  the  probable  termination  of  the 
acute  inflammatory  process  in  chronic  valvular  disease  has  also  to 
be  taken  into  consideration. 

The  condition  of  the  heart  previous  to  the  attack  of  endocarditis 
is  of  considerable  prognostic  importance. 

The  existence  of  old-standing  valvular  disease  greatly  increases 
the  danger  to  life,  and  does  so  in  proportion  to  the  extent  and 
effects  of  the  original  lesion. 

The  presence  of  cardiac  or  pulmonary  complications,  such  as 
pericarditis  and  myocarditis,  or  pleurisy,  pneumonia,  etc.,  also  adds 
greatly  to  the  gravity  of  the  outlook. 

The  site  and  effects  of  the  endocardial  inflammation  form  impor- 
tant elements  in  the  prognosis. 

Speaking  generally,  incompetence  of  the  aortic  valve  is  much 
more  serious  than  insufficiency  of  the  mitral,  whereas  the  danger 
is  reversed  with  respect  to  obstruction  at  these  openings. 

The  estimation  of  the  severity  of  the  lesion  and  its  influence 


148  DISEASES    OF   THE    HEART 

on  the  prognosis  will  be  considered  under  the  head  of  "  Chronic 
Valvular  Affections." 

The  age,  sex,  occupation,  habits,  constitutional  vigour,  and  general 
condition  of  the  patient  must  also  be  taken  into  account  in  forming 
a  prognosis  in  valvular  disease  following  acute  endocarditis,  with  a 
view  to  the  estimation  of  the  amount  of  compensation  that  is  likely 
to  occur,  and  its  probable  duration. 

These  conditions  will  be  more  fully  considered  under  the  account 
of  the  prognosis  of  chronic  valvular  lesions. 

The  time  that  elapses  between  the  subsidence  of  the  acute  process 
and  the  period  at  which  the  patient  resumes  active  exercise  will 
also  materially  affect  the  extent  and  adequacy  of  the  compensatory 
changes. 

TREATMENT 

The  treatment  of  acute  simple  endocarditis  practically  resolves 
itself  into  the  treatment  of  the  disease,  usually  acute  rheumatism, 
on  which  the  cardiac  lesion  depends. 

The  preventive  treatment  of  acute  inflammation  of  the  endo- 
cardium has  hitherto  been  attended  with  httle  success.  Neverthe- 
less the  early  and  active  treatment  of  the  primary  disorder,  and  the 
maintenance  of  absolute  rest,  both  bodily  and  mental,  have  pro- 
bably some  influence  in  warding  off  the  occurrence  of  acute 
endocarditis. 

In  any  case  the  adoption  of  these  precautions  cannot  be  too 
strongly  insisted  upon,  more  especially  with  respect  to  the  manifesta- 
tions of  the  rheumatic  state  in  childhood,  for  the  reasons  which  have 
already  been  given. 

Should  endocarditis  occur,  the  measures  indicated  above  must 
still  be  rigorously  carried  out.  Complete  rest  in  bed  must  be 
enforced,  and  all  sources  of  cardiac  irritation  should,  so  far  as 
possible,  be  removed. 

Light,  easily  digestible  food,  which  should  consist  chiefly  of  milk, 
is  the  most  suitable  diet.  It  is  better  to  avoid  the  use  of  alcohol 
unless  cardiac  failure  supervene. 

The  local  apphcation  to  the  pr^cordium  of  poultices,  fomenta- 
tions, or  a  series  of  flying  blisters  is  sometimes  of  considerable 
service  in  relieving  cardiac  pain  and  distress. 

In  young  plethoric  subjects,  suffering  from  praecordial  pain  and 
oppression,  the  practice  of  venesection — at  one  time  extensively 
employed — has  been  superseded  by  the  use  of  leeches,  of  which 
two  or  four  may  be  placed  on  the  chest  wall  over  the  heart. 

The  local  application  of  an  ice-bag  is  of  great  service  in  allaying 
cardiac  pain  and  distress,  and  in  diminishing  the  general  fever,  but 
this  procedure  must  be  employed  with  caution,  especially  in  weakly 
individuals. 

After   the  subsidence  of  the  acute  symptoms   the   praecordium 


ACUTE     ENDOCARDITIS  149 

may  be  painted  with  a  solution  composed  of  equal  parts  of  the 
tincture  and  liniment  of  iodine.  The  application  should  be  renewed, 
at  intervals  of  three  or  four  days,  for  a  period  of  several  weeks. 

It  is,  as  a  rule,  advisible  in  rheumatic  cases  to  discontinue  the 
use  of  salicylate  of  soda  when  endocarditis  occurs,  on  account  of  the 
depressing  influence  which  this  drug  exerts  on  the  heart.  It  may  be 
replaced  by  the  administration  of  alkalis,  with  which  quinine  and 
sahcin  can  be  combined,  when  necessary,  in  the  form  of  an 
effervescing  mixture. 

Failure  of  the  heart  may  be  met  by  the  use  of  alcohol  and  other 
cardiac  stimulants ;  but  these  remedies  must  be  employed  with 
caution. 

In  some  cases  small  doses  of  digitalis  or  strophanthus,  with  ether 
or  ammonia  and  strychnine,  are  of  great  service  in  quieting  the  heart. 
In  other  instances  of  excited  cardiac  action  the  use  of  anodynes, 
such  as  opium  or  belladonna,  in  small  doses,  is  required. 

Complications  may  be  treated  on  general  principles. 

Rest  should  be  enjoined  for  some  weeks  after  the  subsidence 
of  the  acute  symptoms,  and  convalescence  may  be  hastened  by  the 
use  of  cardiac  and  general  tonics.  Heematinics,  of  which  arsenic  is 
the  most  useful,  are  of  great  service  in  combating  the  ansemia  that 
so  commonly  accompanies  and  follows  an  attack  of  acute  rheu- 
matism. 

Iodide  of  potassium  has  been  given  in  the  later  stages  of  acute 
endocarditis  with  the  object  of  promoting  the  absorption  of  the 
inflammatory  products. 

Exercise  should  be  commenced  cautiously  and  gradually  increased, 
and  care  must  be  taken  for  some  months  to  avoid  sudden  or  violent 
exertion  of  any  kind.  -^^ 

SECTION    II 

MALIGNANT   OR  INFECTIVE   ENDOCARDITIS 

iETIOLOGY 

This  comparatively  rare  form  of  endocarditis  is  most  commonly 
observed  in  connection  with  septic  or  pyemic  conditions.  The 
principal  sources  of  infection  are  septic  wounds,  abscesses,  puerperal 
septic  disease,  suppurative  lesions  of  the  lungs,  liver,  genito-urinary 
passages,  middle  ear,  etc,  and  acute  osteo-myelitis. 

Malignant  endocarditis  of  septic  origin  is  also  found  in  association 
with  acute  and  sub-acute  rheumatism,  chorea,  malaria,  dysentery, 
etc.,  and  with  some  of  the  acute  infectious  fevers — to  wit,  small-pox, 
diphtheria,  scarlet  and  enteric  fevers. 

Several  cases  have  been  recorded  in  which  infective  endocarditis 
has  been  associated  with  gall  stones,  unaccompanied  by  suppuration, 
in  the  biliary  channels. 


ISO  DISEASES   OF   THE    HEART 

Malignant  endocarditis  is  sometimes  observed  as  a  complication 
of  pneumonia  and  meningitis. 

In  a  few  instances  the  disease  has  followed  traumatic  rupture  of 
the  segment  of  a  valve. 

A  small  proportion  of  the  recorded  cases  of  infective  endocarditis 
has  occurred  independently  of  any  ascertainable  cause. 

Malignant  endocarditis  most  commonly  attacks  young  adults 
between  the  ages  of  fifteen  and  thirty-five  years.  The  disease  is 
rare  after  forty,  but  it  is  not  infrequently  observed  in  children. 
Males  suffer  rather  more  frequently  than  females. 

According  to  Osier,  75  per  cent,  of  the  cases  of  malignant 
endocarditis  are  complicated  by  old-standing  valvular  disease,  which 
must  therefore  be  regarded  as  a  powerful  predisposing  cause  of  the 
affection.  Among  other  predisposing  causes  of  the  disease  may  be 
mentioned  privation,  exposure  to  wet  and  cold,  alcoholic  excesses, 
chronic  exhaustive  disease,  and  the  like. 


PATHOLOGY  AND  MORBID  ANATOMY 

Either  or  both  sides  of  the  heart  may  be  affected  by  malignant 
endocarditis.  In  the  large  majority  of  cases,  however,  the  morbid 
process  is  confined  to  the  left  side  of  the  organ.  Nevertheless,  im- 
plication of  the  right  heart  is,  as  might  be  expected,  more  common 
than  in  the  simple  form  of  the  disease. 

The  valves  are  the  parts  chiefly  affected,  but  it  not  uncommonly 
happens  that  other  portions  of  the  endocardium  are  also  involved  in 
this  variety  of  endocarditis. 

The  mitral  valve  is  attacked  rather  more  frequently  than  the  aortic, 
and  it  is  not  unusual  for  both  to  suffer  simultaneously. 

The  morbid  appearances,  so  far  as  the  heart  is  concerned,  are 
characterized  by  a  more  or  less  luxuriant  growth  of  vegetations  on 
the  valves,  and  occasionally  on  neighbouring  parts,  and  by  the 
presence  of  a  variable  though  usually  considerable  degree  of  ulcera- 
tion of  the  valvular  structures  and  adjacent  portions  of  the  endo- 
cardium. Two  main  types  of  malignant  endocarditis  are  sometimes 
distinguished,  according  as  the  vegetative  or  ulcerative  process 
predominates. 

The  vegetations  on  the  valves  are  usually  very  abundant,  exceed- 
ingly friable,  and  of  a  dull  grey  colour.  They  present,  as  a  rule,  a 
characteristic  granular,  fungating,  ragged  appearance. 

The  vegetations  are  often  more  or  less  deeply  ulcerated,  but  the 
loss  of  substance  may  not  be  very  apparent  owing  to  its  replacement 
by  greyish  or  greenish  coloured  blood  clot. 

The  endocardium  is  frequently  found  abraded  in  places,  and  in 
many  instances  the  valves  and  the  parts  adjacent  to  them  are  the 
seat  of  deep  and  extensive  ulcerations,  which  have  an  irregular 
outline  and  an  uneven  greyish  yellow  base. 


ACUTE   ENDOCARDITIS  151 

The  edges  of  the  ulcers  are  commonly  thickened  and  more  or 
less  undermined,  while  their  floors  are  often  wholly  or  partially 
covered  by  blood  clot. 

Ulceration  is  not,  however,  invariably  present.  It  is  most  com- 
monly observed  in  those  cases  in  which  malignant  endocarditis  has 
attacked  a  valve  that  is  already  the  seat  of  inflammatory  or  sclerotic 
changes. 

The  action  of  the  ulcerative  process  on  the  valves  is  usually 
followed  by  the  most  disastrous  results,  among  which  are  aneurism, 
perforation  or  rupture  of  the  valvular  segments.  In  some  instances 
the  cusps  of  a  valve  undergo  more  or  less  complete  destruction. 
Ulceration,  and  rupture  of  the  chordae  tendine^,  is  sometimes 
observed,  and  may  lead  to  the  detachment  of  a  valvular  curtain. 
The  flapping  of  the  loosened  segment  against  the  wall  of  the  heart, 
with  each  systole,  may  give  rise  to  fresh  centres  of  infection  at  the 
sites  of  impact. 

Ulceration  of  the  endocardium  lining  the  cavities  of  the  heart 
may  result  in  aneurism,  abscess,  or  even  rupture  of  the  muscular 
wall  of  the  organ. 

Perforation  of  the  septum  ventriculorum  has  been  recorded  in  a 
few  instances. 

Ulceration  at  the  root  of  the  aorta,  consequent  on  the  extension 
of  the  inflammatory  process  from  the  aortic  valve,  may  be  followed 
by  aneurism  and  rupture  of  the  vessel  wall. 

In  addition  to  the  changes  just  mentioned,  evidence  of  pre- 
existent  valvular  disease,  with  enlargement  of  the  heart,  is  found  in 
three-quarters  of  the  cases  of  malignant  endocarditis.  In  a  few 
instances  the  heart  has  been  the  seat  of  a  congenital  malformation. 

Acute  pericarditis,  too,  sometimes  complicates  malignant  endo- 
carditis. 

On  microscopical  examination  the  endocardial  inflammatory 
changes  resemble  for  the  most  part  those  seen  in  the  simple  form 
of  the  disease.  In  malignant  endocarditis,  however,  micro-organisms 
of  various  kinds  are  always  found  distributed  throughout  the  vegeta- 
tions and  along  the  floor  of  the  ulcers  to  a  varying  depth.  They 
are  often  collected  into  masses,  and  are  usually  most  numerous  at 
the  periphery  of  the  vegetations.  The  kind  of  micro-organism 
found  is  not  the  same  in  all  cases,  and  a  large  variety  of  pathogenic 
and  non-pathogenic  forms  have  been  observed  at  different  times. 
The  pathogenic  forms  which  have  been  shown  to  be  capable  of 
exciting  endocarditis  are  the  Staphylococcus  pyogenes  aureus,  and 
albus,  the  Streptococcus  pyogeties,  the  Diplococcus  pneumonice,  and  a 
bacillus  discovered  by  Gilbert  and  Lyon. 

Malignant  endocarditis  has  occasionally  been  ascribed  to  the 
bacilli  of  tuberculosis,  enteric  fever,  and  diphtheria,  and  to  the 
gonococcus.  The  occurrence  of  infective  endocarditis  in  the  course 
of  these  affections  is,  however,  usually  due  to  septic  organisms,  which 
also  commonly  accompany  the  diseases  in  question.     It  is  probable, 


152  DISEASES   OF   THE    HEART 

too,  that,  in  some  instances,  the  cardiac  lesion  depends  on  the  com- 
bined action  of  both  sets  of  micro-organisms. 

Certain  special  forms  of  micro-organisms  have  been  described  in 
connection  with  malignant  endocarditis,  as,  for  instance,  the  Bacillus 
endocarditis  rugatus,  the  Bacillus  endocarditis  capsulatus,  and  the 
Bacillus  endocarditis  griseus  of  Weichselbaum,  and  the  Bacillus 
iminobilis  et  fcetidus  of  Frankel  and  Saenger.  The  pathological 
significance  of   these  organisms  is  not  yet  understood. 

In  most  instances  only  one  micro-organism  is  found,  but  oc- 
casionally the  CO -existence  of  several  different  kinds  has  been 
observed. 

It  would  appear,  therefore,  that  the  organisms  most  commonly 
concerned  in  the  production  of  malignant  endocarditis  are  those 
found  in  connection  with  septic  and  pysemic  conditions  and  with 
pneumonia.  Pneumonic  endocarditis,  however,  is  sometimes  due 
to  a  mixed  infection. 

Two  views  are  held  with  respect  to  the  manner  in  which  the 
micro-organisms  gain  access  to  the  valves.  The  opinion  expressed 
by  the  majority  of  observers  is  that  the  microbes  are  deposited  from 
the  blood  on  to  the  free  surface  of  the  valves,  and  there  fructify. 
Others  consider  that  the  organisms  are  carried  into  the  blood  vessels 
of  the  valves,  where  they  form  emboli,  which  serve  as  centres  for  the 
progagation  of  the  infection  to  the  surface.  The  latter  view  has 
been  opposed  on  the  ground  that  the  valves,  for  the  most  part, 
are  destitute  of  blood  vessels.  This  objection  is  not  good,  however, 
in  cases  of  chronic  inflammation  of  the  endocardium,  inasmuch  as, 
under  these  circumstances,  the  diseased  valves  are  abundantly  sup- 
plied with  blood  vessels.  Moreover,  embolic  collections  of  micro- 
organisms have  been  seen  in  the  vessels  of  the  inflamed  valves  by 
several  observers.  It  is  possible,  as  Dreschfeld  suggests,  that  both 
methods  of  infection  of  the  valves  may  obtain. 

In  addition  to  the  cardiac  lesions  which  have  been  described, 
malignant  endocarditis  is  associated  with  a  variety  of  other  morbid 
conditions.  The  most  important  of  these  is  embolism,  which,  from 
both  a  pathological  and  clinical  point  of  view,  is  one  of  the  charac- 
teristic features  of  malignant  endocarditis. 

If  the  endocarditis  affect  the  left  side  of  the  heart,  infarction  of 
the  spleen,  kidneys,  heart,  brain,  liver,  intestines,  skin,  and  retina  is 
of  common  occurrence.  When  the  lesion  is  right-sided,  embolism 
and  abscess  of  the  lungs  are  observed. 

It  occasionally  happens,  more  especially  in  the  vegetative  form 
of  the  disease,  that  a  large  vessel  such  as  the  middle  cerebral, 
mesenteric,  brachial,  or  femoral  artery,  or  even  the  abdominal  aorta, 
becomes  occluded. 

The  infarcts,  in  some  instances,  break  down  with  the  formation 
of  local  abscesses,  in  which  micro-organisms  similar  to  those  already 
noticed  in  the  valvular  vegetations  may  often  be  detected. 

The   stomach   and   intestines   are   not   infrequently  the   seat  of 


ACUTE   ENDOCARDITIS     '  153 

haemorrhagic  infarcts,  with  congestion  and  ulceration  of  the  mucous 
membrane.  Gangrene  of  a  portion  of  the  intestine  has  been  ob- 
served to  follow  the  occlusion  of  a  large  branch  of  the  mesenteric 
artery. 

Inflammation  of  the  serous  membranes,  especially  in  the  form  of 
pleurisy  with  purulent  effusion,  is  not  uncommon. 

Croupous  pneumonia,  usually  of  a  septic  type,  may  precede  or 
follow  the  cardiac  lesion. 

Suppurative  meningitis  and  cerebral  haemorrhage  are  occasionally 
observed. 

Micro-organisms  can  sometimes  be  discovered  in  the  circulating 
blood,  and  septic  thrombi  may  be  found  in  the  vessels  after  death. 

Granular  degeneration  of  the  heart,  liver,  and  kidneys  are  in- 
variably found  in  association  with  malignant  endocarditis. 

The  primary  affection  may  or  may  not  be  obtrusive.  As  a  rule, 
however,  one  or  other  of  the  morbid  conditions  mentioned  under 
the  head  of  "Etiology"  is  found  in  connection  with  the  cardiac 
lesion. 

SYMPTOMS 

The  clinical  phenomena  associated  with  malignant  endocarditis 
vary  greatly  in  different  cases.  Moreover,  the  symptoms  due  to  the 
cardiac  inflammation  are  frequently  insignificant,  and  are  apt  to  be 
overshadowed  by  those  of  the  general  infection.  It  is  customary, 
from  a  clinical  point  of  view,  to  distinguish  an  acute  form,  and  a 
sub-acute  or  chronic  form  of  the  disease.  It  must,  however,  be 
clearly  understood  that  many  cases  of  an  intermediate  kind  occur, 
which  do  not  conform  exactly  to  either  of  these  types.  Neverthe- 
less, this  division  of  the  subject  will,  with  the  reservation  just  men- 
tioned, be  adopted  as  the  most  suitable  for  descriptive  purposes. 

Two  varieties  of  the  acute  form  of  malignant  endocarditis  are 
recognised  according  as  the  symptoms  assume  a  typhoid  or  septic 
character. 

The  TYPHOID  variety  of  the  disease  sometimes  commences  sud- 
denly with  one  or  more  rigors,  followed  by  headache,  vomiting, 
rise  of  temperature,  and  grave  constitutional  disturbance.  In  other 
instances  the  onset  is  gradual,  and  takes  the  form  of  slowly  in- 
creasing prostration,  accompanied  by  a  variable  degree  of  pyrexia 
and  ill-developed  cardiac  signs  and  symptoms. 

The  patient  quickly  passes  into  an  apathetic  state,  which  is 
attended  by  profound  prostration,  profuse  sweating,  and  general 
muscular  tremor. 

The  tongue,  which  is  furred  at  first,  becomes  dry,  brown,  and 
fissured.  Sordes  form  on  the  lips  and  gums.  The  bowels  become 
relaxed,  and  melsena  is  not  uncommon.  Tympanites  usually 
appears ;  the  spleen  is  invariably  enlarged  and  tender ;  and  the 
urine  frequently  contains  albumen  and  sometimes  blood. 


154  DISEASES   OF  THE   HEART 

The  breathing  is  hurried  and  shallow,  and  cough  may  be  attended 
by  hemorrhagic  expectoration. 

The  fever  is  usually  high  (103-105°  F.)  and  of  a  continued  type, 
with  small  daily  remissions.  In  some  of  the  most  rapidly  fatal  cases, 
however,  the  temperature  does  not  rise  above  100°  F. 

Symptoms  due  to  embolism  of  the  brain,  spleen,  kidneys,  or  skin 
may  appear  at  any  period  of  the  attack. 

Rashes  of  an  erythematous,  papular,  purpuric,  or  even  pustular 
character  are  frequently  seen  on  the  skin. 

Optic  neuritis  and  retinal  haemorrhages  are  not  uncommon. 

Meningitis,  associated  with  headache,  drowsiness,  and  coma,  01 
with  delirium  and  convulsions,  is  sometimes  observed. 

Other  compHcations  commonly  found  are  pericarditis,  pleurisy, 
empyema,  suppurative  arthritis,  and  jaundice. 

The  cardiac  symptoms  are  usually  indefinite,  but  occasionally  the 
patient  complains  of  palpitation  and  prsecordial  uneasiness  or  pain. 
In  exceptional  instances  urgent  dyspnoea,  dropsy,  and  other  evidence 
of  mechanical  derangement  of  the  circulation  is  observed. 

The  pulse  is  rapid  at  first,  and  often  markedly  dicrotic ;  in  the 
later  stages  of  the  disease  it  becomes  small,  weak,  and  almost 
imperceptible. 

The  sounds  of  the  heart  are  usually  weak,  and  may  be  accom- 
panied by  murmurs,  which  are  commonly  systolic  in  the  mitral,  and 
diastolic  in  the  aortic  area.  A  bruit  is  occasionally  audible  over 
the  right  side  of  the  heart.  The  character  of  the  murmurs  frequently 
changes  from  day  to  day,  or  even  while  under  observation. 

It  is  sometimes  possible  to  elicit  the  signs  of  dilatation  of  the  heart. 

The  duration  of  the  disease  is  usually  short.  Death  takes  place, 
as  a  rule,  within  fourteen  days  from  cardiac  failure,  or  from  the 
effects  of  the  general  infection,  or  of  embolism,  or  of  some  other 
complication.  A  fatal  termination  has  been  observed  on  the  second 
day  of  the  disease.  In  very  rare  instances  the  affection  assumes  a 
sub-acute  or  chronic  character. 

The  SEPTIC  or  PY^.MIC  form  of  mahgnant  endocarditis 
commences  suddenly  with  severe  and  repeated  rigors,  followed 
by  profuse  sweating.  The  temperature,  which  is  usually  high 
and  extremely  irregular,  may  be  of  the  remittent  or  intermittent 
tj'pe  of  pyrexia. 

The  tongue  is  furred  at  the  outset,  but  tends  later  on  to  become 
brown  and  dry.  There  is  commonly  great  thirst,  and  more  or  less 
complete  anorexia,  while  vomiting  is  often  a  troublesome  symptom. 
Tympanites  and  diarrhoea  are  frequently  observed,  and  the  spleen 
is  almost  invariably  enlarged.  The  respirations  are  quick  and 
shallow,  and  the  pulse,  which  is  often  irregular,  is  rapid  and  easily 
compressible. 

Embolic  manifestations  are  of  common  occurrence,  and  meta- 
static abscesses  may  appear  in  divers  situations.  The  skin  may  show 
any  of  the  rashes  previously  mentioned. 


ACUTE   ENDOCARDITIS  15S 

Meningitis,  with  headache,  delirium,  coma,  etc.,  is  an  important 
and  common  complication  of  this  form  of  malignant  endocarditis. 

Suppurative  inflammation  of  the  serous  membranes  and  joints, 
pneumonia,  nephritis,  and  jaundice  are  other  complications  which 
are  not  infrequently  observed. 

A  physical  examination  of  the  heart  seldom  discovers  any  dis- 
tinctive indication  of  the  endocardial  lesion. 

The  cardiac  impulse  is  usually  feeble,  and  there  may  or  may  not 
be  evidence  of  dilatation  of  the  heart.  Systolic  murmurs  are 
frequently  audible  in  the  mitral  and  tricuspid  areas,  but  they  do 
not  differ  materially  from  the  bruits  which  are  commonly  heard,  in 
the  absence  of  endocardial  disease,  during  the  course  of  many  of 
the  acute  febrile  disorders. 

This  variety  of  malignant  endocarditis  usually  runs  a  rapid  course, 
in  that  a  fatal  termination  is  seldom  delayed  beyond  a  fortnight  or 
three  weeks. 

The  sub-acute  and  chronic  variety  of  malignant  endocarditis  is 
termed  also  the  "cardiac"  or  "malarial"  type  by  some  authors. 
It  occurs  in  association  with  old-standing  valvular  affections  of  the 
heart,  and  is  the  form  in  which  malignant  endocarditis  most  com- 
monly appears. 

The  disease  generally  begins  insidiously,  but  in  a  few  instances  a 
more  or  less  acute  onset  is  observed. 

In  the  usual  course  of  events  the  patient,  who  is  already  the 
subject  of  a  valvular  affection  of  the  heart,  complains  of  general 
malaise.  He  becomes  anaemic,  begins  to  waste,  and  develops  an 
irregular  pyrexia,  which  is  sooner  or  later  accompanied  by  the  signs 
and  symptoms  of  multiple  embolism. 

In  other  instances,  after  a  longer  or  shorter  spell  of  ill  health,  the 
patient  is  suddenly  seized  with  a  rigor,  followed  by  sweating,  which 
may  be  repeated  at  irregular  intervals  over  a  period  of  weeks  or 
months. 

Whatever  be  the  mode  of  onset,  the  main  features  of  this  type  of 
malignant  endocarditis  are  the  presence  of  an  endocardial  lesion,  in 
association  with  pyrexia,  of  a  very  fluctuating  character,  and  multiple 
embolism.  A  physical  examination  of  the  heart  shows  the  existence 
of  cardiac  enlargement  and  the  presence  of  a  murmur  in  the  mitral 
or  aortic  area,  or  in  both  these  situations.  In  rare  instances  evidence 
of  right-sided  endocarditis  is  obtained. 

The  murmurs,  whether  systolic  or  diastoHc,  often  develop  sud- 
denly, and  they  not  infrequently  undergo  changes  in  character  during 
the  course  of  the  disease. 

The  fever  associated  with  this  variety  of  malignant  endocarditis 
sometimes  assumes  a  remittent  or  intermittent  type,  while,  in  other 
instances,  it  is  more  or  less  continuous,  with  occasional  irregular 
exacerbations. 

The  occurrence  of  embolism  is  a  constant  and  important  feature 
of  the  chronic  form  of  malignant  endocarditis. 


156  DISEASES   OF   THE    HEART 

Infarcts  are  consequently  produced  in  various  organs,  and,  in  the 
event  of  the  emboU  possessing  infective  properties,  suppurative 
inflammation  of  the  area  of  infarction  takes  place,  with  the  forma- 
tion of  metastatic  abscesses. 

Embolic  infarction  of  the  brain,  spleen,  kidneys,  or  skin  may  be 
respectively  indicated  by  hemiplegia  with  deHrium,  coma  and  con- 
vulsions ;  pain  and  tenderness  in  the  splenic  area ;  hematuria ;  and 
purpuric  rashes  on  the  skin. 

The  occurrence  of  pain  in  the  chest,  shortness  of  breath,  and  the 
spitting  of  blood,  would  point  to  infarction  of  the  lungs. 

EmboHsm  of  the  myocardium  may  be  followed  by  grave  cardiac 
symptoms. 

It  occasionally  happens  that  an  artery  supplying  a  limb  becomes 
blocked.  In  this  event  pulsation  is  abolished  on  the  distal  side 
of  the  plug,  and  the  limb  becomes  cold  and,  in  rare  instances, 
gangrenous. 

Embolism  of  the  mesenteric  artery,  which  has  been  observed  in  a 
few  cases,  is  accompanied  by  severe  pain  in  the  abdomen,  melaena, 
and  collapse. 

Inflammation  of  the  joints,  with  or  without  suppuration,  is  not 
uncommonly  observed,  and  is  probably  of  embolic  origin. 

An  ophthalmoscopic  examination  may  show  retinal  hsemorrhages 
or  optic  neuritis,  or  both  these  lesions. 

The  serous  and  mucous  membranes  are  frequently  the  seat  of 
inflammatory  changes,  and  bleeding  may  take  place  from  their  free 
surfaces. 

The  spleen  is  usually  enlarged,  independently  of  the  occurrence  of 
infarction  of  the  organ. 

In  some  instances  the  liver  is  also  increased  in  size,  while  slight 
jaundice  is  not  uncommon. 

The  urine,  which  is  frequently  diminished  in  quantity,  deposits 
lithates  on  standing.  It  is  often  albuminous,  and  sometimes  con- 
tains blood. 

The  more  important  complications  are  pleurisy  and  pneumonia; 
pericarditis,  meningitis,  cerebral  haemorrhage,  and  acute  aneurism. 

The  duration  of  this  type  of  malignant  endocarditis  varies  between 
a  few  weeks  and  a  few  months.  In  exceptional  instances  the  disease 
has  lasted  for  more  than  a  year.  Recovery  is  extremely  rare,  but  in 
a  few  cases  this  result  has  been  recorded. 

PHYSICAL  SIGNS 

The  cardiac  physical  signs  which  may  be  found  in  connection 
with  mahgnant  endocarditis  will  be  briefly  recapitulated. 

The  information  afforded  by  a  physical  examination  of  the  heart 
in  cases  of  this  disease  is,  as  a  rule,  inconclusive,  and  considered 
apart  from  the  general  condition  of  the  patient  is  seldom  of  much 
diagnostic  value.     The  presence,  however,    of  a   cardiac   murmur 


ACUTE  ENDOCARDITIS  157 

of  doubtful  nature  in  association  with  irregular  pyrexia  and  grave 
constitutional  symptoms  renders  the  existence  of  malignant  endo- 
carditis exceedingly  probable. 

Mitral  murmurs  occurring  in  this  form  of  endocarditis,  in  the 
absence  of  pre-existent  valvular  disease,  are  usually  systolic  in  time, 
soft  and  blowing  in  character,  and  audible  in  the  neighbourhood 
of  the  apex  only.  The  sudden  appearance  of  a  bruit  of  this 
description,  which  alters  in  character  from  day  to  day,  should 
alwaj's  lead  to  a  suspicion  of  malignant  endocarditis  in  a  febrile 
disorder  of  uncertain  nature. 

Aortic  murmurs  may  be  either  systolic  or  diastolic,  but  they  are 
seldom  well  developed. 

In  those  cases  in  which  endocarditis  of  a  malignant  type  attacks 
a  heart,  already  the  seat  of  a  valvular  affection,  a  change  may 
be  observed  in  the  character  of  the  murmur,  previously  noticed, 
or  the  extension  of  the  morbid  process  to  another  orifice  may  lead 
to  the  sudden  development  of  a  bruit  in  a  new  situation. 

Rapid  failure  of  the  heart,  with  all  the  signs  and  symptoms  of 
acute  derangement  of  the  circulation,  is  sometimes  observed  in 
cases  of  malignant  endocarditis.  In  other  instances  the  cardiac 
dilatation  comes  on  gradually,  and  is  associated  with  passive 
engorgement  and  increase  in  the  size  of  the  liver,  general  venous 
congestion,  and  dropsy. 

DIAGNOSIS 

The  recognition  of  malignant  endocarditis  depends,  as  already 
stated,  on  the  presence  of  variable,  though  usually  indefinite, 
cardiac  phenomena,  in  association  with  irregular  pyrexia,  enlarge- 
ment of  the  spleen,  and  grave  constitutional  symptoms,  which 
frequently  assume  a  typhoid  or  pysemic  character. 

The  disease  has  to  be  distinguished  from  a  variety  of  other  dis- 
orders, chief  among  which  are  acute  simple  endocarditis,  enteric  fever, 
pysemia,  meningitis,  pneumonia,  and  acute  generalized  tuberculosis. 

The  diagnosis  from  acute  simple  endocarditis  is  often  a  matter 
of  little  or  no  difficulty,  but  at  other  times  the  differentiation 
between  the  two  affections  may  be  almost  impossible,  since  cases 
occur  which  combine  features  belonging  to  both  disorders. 

In  the  malignant  form  the  sudden  onset  (typhoid  and  pyaemic 
type),  rapid  prostration,  and  irregular  pyrexia  are  in  marked  contrast 
to  the  insidious  development  and  generally  mild  course  of  the 
simple  variety.  Signs  of  enlargement  of  the  spleen,  the  occurrence 
of  multiple  embolism,  and  evidence  of  acute  nephritis  are  much 
less  seldom  observed  in  the  simple  than  in  the  infective  form 
of  the  disease.  Moreover,  simple  endocarditis  rarely,  if  ever, 
gives  rise  to  typhoid  or  pytemic  symptoms.  Furthermore,  a  rapid 
development  and  a  changeable  character  of  the  cardiac  physical  signs 
are  more  distinctive  of  the  malignant  than  of  the  benign  variety 
of  endocarditis. 


iS8  DISEASES    OF    THE    HEART 

A  blood  count  is  not  of  very  great  service  in  the  differential 
diagnosis  of  acute  simple  and  acute  infective  endocarditis  inasmuch 
as  a  leucocytosis  has  been  observed  in  both  forms  of  the  disease. 
Speaking  generally  a  pronounced  leucocytosis  is  in  favour  of  the 
existence  of  the  infective  variety.  Nevertheless  the  occurrence  of 
septic  phenomena  in  association  with  cardiac  symptoms,  even  in 
the  absence  of  leucocytosis,  is  indicative  of  infective  endocarditis. 

Finally,  the  presence  of  micro-organisms,  usually  in  the  form 
of  streptococci,  which  are  sometimes  observed  in  the  circulating 
blood,  would  be  conclusive  evidence  in  favour  of  malignant 
endocarditis. 

The  diagnosis  of  malignant  endocarditis  from  enteric  fever  is 
often  very  difficult,  but  the  insidious  onset,  the  characteristic  rise 
of  temperature,  and  the  more  gradual  prostration  of  enteric  fever 
afford  important  evidence  in  the  differentiation  of  the  two  diseases. 
Cardiac  and  circulatory  phenomena  occur  earlier,  and  are,  as  a  rule, 
better  developed  in  malignant  endocarditis  than  in  enteric  fever. 
Symptoms  of  multiple  embolism,  or  acute  nephritis,  would  tell 
in  favour  of  the  endocardial  affection.  Diarrhoea,  tympanites,  and 
rose  spots  on  the  abdomen  render  enteric  fever  more  probable.  The 
skin  eruptions  occurring  in  malignant  endocarditis  can  usually 
be  distinguished  from  those  of  enteric  fever  by  a  careful  examina- 
tion. The  early  appearance  of  cerebral  symptoms  or  of  eye  pheno- 
mena would  be  greatly  in  favour  of  malignant  endocarditis. 

The  existence  of  a  leucocytosis  negatives  the  presence  of  enteric 
fever.  The  application  of  the  Widal  serum  test  would  clench  the 
diagnosis  in  a  doubtful  case. 

The  differential  diagnosis  between  malignant  endocarditis  and 
pygemia  is  often  impossible,  since,  as  has  already  been  pointed  out, 
the  two  affections  are  to  all  intents  and  purposes  identical.  The 
occurrence  of  multiple  embolism  and  the  absence  of  a  primary 
suppurating  focus  would  make  for  a  diagnosis  of  malignant  en- 
docarditis. 

The  means  of  distinguishing  between  malignant  endocarditis  and 
meningitis  are  found  in  the  history  and  mode  of  onset  of  the  two 
affections,  and  in  the  more  common  occurrence  of  such  symptoms 
as  squint,  optic  neuritis,  retraction  of  the  head  or  abdomen,  muscular 
spasm  and  paralysis  in  the  latter  disorder. 

The  diagnosis  of  malignant  endocarditis  from  pneumonia  has  to 
be  made  in  those  cases  in  which  inflammation  of  the  lungs  com- 
plicates pre-existent  valvular  disease  of  the  heart. 

The  differential  diagnosis  rests  on  the  whole  history  of  the 
attack,  and  each  case  must  be  decided  on  its  merits,  though  it  is 
sometimes  impossible  to  come  to  a  definite  conclusion. 

Acute  generalized  tuberculosis  may  closely  resemble  malignant 
endocarditis. 

In  attempting  to  make  a  differential  diagnosis,  the  history  and 
mode  of  onset  of  the  attack  and  the  presence  or  absence  of  a  focus 
of  tubercular  dissemination  must  be  taken  into  consideration.  The 
existence  of  choroidal  tubercle,  or  the  appearance  of  tubercle  bacilli 


ACUTE    ENDOCARDITIS  159 

in  the  sputum,  would  render  the  diagnosis  easy.  The  signs  of  cardiac 
disease,  of  multiple  embolism,  and  of  acute  nephritis  would  be 
greatly  in  favour  of  malignant  endocarditis.  Skin  eruptions,  too, 
are  more  common  in  the  endocardial  affection  than  in  acute 
generalized  tuberculosis. 

PROGNOSIS 

The  prognosis  in  the  acute  forms  of  malignant  endocarditis  is 
most  unfavourable. 

Life  is  seldom  prolonged  much  beyond  a  fortnight,  and  a  fatal 
issue  frequently  takes  place  within  a  week. 

The  chronic  variety  of  the  disease  affords  a  slightly  less  unfavour- 
able outlook,  since  recovery  has  been  recorded  in  a  few  undoubted 
cases  of  this  kind. 

It  is  possible,  however,  that  the  application  of  recent  methods 
of  treatment  will  materially  reduce  the  mortality  from  malignant 
endocarditis. 

TREATMENT 

The  therapeutic  measures  employed  in  septic  and  pyasmic 
conditions  are  equally  adapted  for  the  treatment  of  malignant 
endocarditis. 

Moreover,  the  various  precautions  mentioned  under  the  treatment 
of  the  simple  form  of  the  disease  should  also  be  adopted. 

Rest,  warmth,  and  abundance  of  fresh  air  are  of  the  first  im- 
portance. The  diet  should  consist  of  concentrated  liquid  food,  given 
in  small  quantities  at  frequent  intervals. 

Free  stimulation  by  means  of  alcohol,  ether,  ammonia  is  usually 
required,  and  should  be  combined  v/ith  the  administration  of  digitalis, 
strychnine,  and  other  cardiac  or  general  tonics. 

Antiseptic  remedies  in  the  form  of  quinine,  salol,  perchloride  of 
mercury,  the  sulpho-carbolates,  etc.,  have  been  extensively  used, 
but  with  little  or  no  advantage. 

Medication  by  means  of  blood  serums  has  recently  been  tried, 
and  appears  likely  to  give  better  results  than  have  hitherto  been 
obtained  in  the  treatment  of  malignant  endocarditis. 

The  kind  of  serum  employed  varies  with  the  form  of  infection 
which  obtains,  but  since  the  large  majority  of  cases  of  malignant 
endocarditis  are  due  to  pyogenic  organisms,  the  anti-streptococcus 
serum  is  most  commonly  indicated. 

Several  cases  of  malignant  endocarditis  successfully  treated  by 
this  serum  have  already  been  published,  and  although  the  results 
so  far  obtained  have  not  been  uniformly  favourable,  they  are 
sufficiently  encouraging  to  warrant  a  further  trial  of  this  method 
of  treatment. 

Benefit  has  apparently  been  derived  in  a  few  cases  from  the 
hypodermic  administration  of  pure  cultures  of  yeast,  or  of  yeast- 
nuclein,  but  it  cannot  be  said  that  this  method  of  treatment  affords 
much  better  results  than  many  of  the  other  remedial  measures 
that  have  been  tried. 


CHAPTER   IX 
CHRONIC   ENDOCARDITIS 

Pathogenesis — Morbid  Anatomy — Effects  on  the  Functions  of  the  Valves — Effects 
on  the  Heart  and  Circulation — Effects  on  other  organs. 

Chronic  endocarditis  is  commonly  the  sequel  of  an  acute  or  sub- 
acute inflammation  of  the  endocardium,  but  in  a  large  number  of 
instances  the  morbid  process  develops  gradually  and  insidiously, 
and  is  chronic  from  the  beginning. 

Rheumatism  is  by  far  the  most  common  cause  of  chronic  endo- 
carditis in  persons  under  middle  age.  During  and  after  this  period 
of  life  chronic  inflammation  of  the  endocardium  (which  gradually 
merges  into  and  becomes  indistinguishable  from  the  morbid  con- 
dition known  as  atheroma  or  arterio-sclerosis)  usually  depends  on 
the  strain  imposed  on  the  valves  and  walls  of  the  heart  by  long- 
continued  or  recurrent  high  blood  pressure  in  the  aorta.  The 
walls  of  this  vessel  suffer  in  common  with  the  heart,  and  in  many 
instances  are  the  primary  seat  of  the  inflammatory  or  degenerative 
changes.  Excessive  blood  pressure  in  the  aorta  is  most  commonly 
due  to  the  protracted  high  arterial  tension  that  is  associated  with 
renal  disease,  gout,  chronic  poisoning  by  lead  or  alcohol,  excessive 
eating  and  drinking,  and  the  defective  elimination  of  the  waste 
products  of  metabolism,  old  age,  and  other  conditions.  It  is  also 
produced  by  muscular  strain,  more  especially  when  the  effort  is 
made  in  a  constrained  position  or  is  accompanied  by  fixation  of  the 
chest  and  closure  of  the  glottis,  as  in  the  case  of  miners,  colliers, 
navvies,  wharfingers,  etc.  Here,  although  the  stress  is  intermittent, 
it  acts  at  times  A^dth  great  intensity,  and  frequently  obtains  over  a 
considerable  number  of  years. 

Syphilis,  chronic  alcoholism,  and  excessive  eating  and  drinking, 
etc.,  which  are  potent  factors  in  the  causation  of  atheroma,  no  doubt 
frequently  co-operate  with  strain  in  the  production  of  degenerative 
or  chronic  inflammatory  lesions  of  the  cardiac  valves.  It  is  probable, 
too,  that  both  gout  and  syphilis  occasionally  act  as  direct  exciting 
causes  of  endocarditis. 

The  influence  of  chlorosis  in  the  causation  of  chronic  valvular 
changes  must  be  ascribed  to  the  high  arterial  tension  which  is 
sometimes  found  in  association  with  this  disorder. 

Mental  excitement  or  w^orry,  and  prolonged  acceleration  of  the 

1 60 


CHRONIC    ENDOCARDITIS  i6i 

heart's  action,  when  combined  with  strain,  may  also  be  mentioned 
as  occasional  causes  of  chronic  valvular  changes. 

In  some  instances  endocarditis  has  followed  external  violence  in 
the  shape  of  a  blow  or  fall  on  the  chest. 

Rupture  of  a  valve  and  subsequent  valvulitis  is  occasionally  pro- 
duced by  sudden  muscular  effort. 


PATHOLOGY  AND  MORBID  ANATOMY 

As  in  the  acute  form  of  the  disease,  the  valvular  structures  on 
the  left  side  of  the  heart  are  the  parts  most  commonly  affected. 
Right-sided  valvular  lesions  are  seldom  observed,  except  as  the 
result  of  diseases  of  the  lungs  or  left  heart,  and  in  some  instances 
of  foetal  endocarditis,  or  congenital  malformation.  The  rarity  of 
post-natal  inflammatory  affections  of  the  pulmonic  and  tricuspid 
valves  has  already  been  accounted  for  under  the  pathology  of  acute 
endocarditis. 

Chronic  endocarditis  of  the  mitral  valve  is  usually  of  rheumatic 
origin. 

The  aortic  valve,  on  the  other  hand,  suffers  more  commonly  from 
the  effects  of  strain.  In  any  event,  strain  tends  to  perpetuate  and 
aggravate  chronic  inflammatory  or  degenerative  changes  affecting 
either  the  mitral  or  aortic  valve. 

The  morbid  process  in  chronic  endocarditis  consists  primarily  in 
a  gradual  fibrosis  of  the  valves  and  their  attachments,  which,  in 
consequence,  become  thickened,  hard,  and  rigid.  The  subsequent 
contraction  of  the  newly  formed  fibrous  tissue  leads  to  a  variety 
of  issues,  among  which  are  narrowing  of  the  valvular  orifices, 
puckering,  retraction,  and  distortion  of  the  curtains  of  the  valves, 
and  shortening  of  the  chordse  tendineae. 

The  thickened  endocardium  is  very  liable  to  be  attacked  by 
atheroma,  or  the  disease  may  have  been  originally  of  an  atherom- 
atous nature,  and  in  either  event  the  affected  structures  are  com- 
monly the  seat  of  ulceration  and  calcification. 

Ulcerative  lesions  lead  to  thinning,  or  even  to  perforation  of  the 
valvular  curtains,  and  it  sometimes  happens  that  the  flap  of  a  valve 
becomes  partially  or  wholly  destroyed  by  the  extension  of  this  process. 

In  other  instances  the  aortic  orifice,  less  commonly  the  mitral 
opening,  is  converted  into  a  calcareous  ring,  and  the  segments  of 
the  valves  not  infrequently  undergo  a  similar  transformation. 

The  aortic  valve  is  especially  liable  to  atheromatous  changes, 
owing  to  the  frequent  extension  of  the  morbid  process  from  the 
root  of  the  aorta.  The  disease  may  in  like  manner  spread  from 
the  aortic  to  the  mitral  valve. 

Acute  endocarditis  often  attacks  the  sclerosed  and  degenerated 
tissue,  and  may  give  rise  to  vegetations  which  are  sometimes  a 
source  of  embolism. 


i62  DISEASES    OF   THE    HEART 

The  endocardial  changes  in  chronic  endocarditis  are  not  neces- 
sarily confined  to  the  cardiac  valves. 

Patches  of  thickened  tissue  are  often  found  in  other  parts  of  the 
lining  membrane  of  the  heart,  and  these  may  become  atheromatous, 
and  in  some  instances  ulcerate,  or  undergo  a  calcareous  transforma- 
tion. 

EFFECTS  ON  THE  FUNCTIONS  OF  THE 
VALVES 

The  effect  of  chronic  endocarditis  is  to  impair  to  a  greater  or  less 
extent  the  functional  efficiency  of  the  valvular  apparatus  of  the 
heart,  and  thus  to  interfere  with  the  normal  circulation  of  blood 
through  the  organ. 

The  valvular  inefficiency  may  take  one  of  three  directions,  i.e. 
the  damaged  cusps  may  be  unable  to  completely  close  the  orifice 
which  they  guard,  or  the  orifice  itself  miay  be  narrowed,  or,  as  most 
commonly  happens,  the  two  conditions  are  combined  in  varying 
proportions. 

In  the  first  event  the  valve  permits  the  backward  flow  of  blood, 
and  is  said  to  be  incompetent;  in  the  second  the  onward  flow  of 
blood  is  hindered,  and  the  term  "stenosis"  or  obstruction  is  applied 
to  the  condition  of  the  opening. 

Incompetence  of  a  valve  may  occur  without  obstruction  at  the 
orifice  which  it  guards,  as  the  result  either  of  retraction  or  ulcera- 
tion of  the  valvular  curtains. 

Obstruction  at  an  orifice,  on  the  other  hand,  is  very  commonly 
attended  by  some  degree  of  incompetence  of  its  valve,  owing  to  the 
usual  inability  of  the  valvular  cusps,  whether  damaged  or  not,  to 
adequately  close  the  narrowed  opening. 

EFFECTS  ON  THE  HEART  AND  CIRCULATION 

Organic  valvular  disease  of  the  heart,  whether  obstructive  or 
regurgitant,  tends  to  produce  anaemia  in  front  and  congestion 
behind  the  seat  of  the  lesion.  This  result  is,  however,  seldom 
very  obvious  at  first,  except  in  cases  where  incompetence  of  a  valve 
is  suddenly  produced,  owing  to  the  estabUshment  of  compensatory 
changes,  which  temporarily,  at  least,  restore  the  balance  of  the 
circulation. 

Compensatory  changes  always  entail  some  degree  of  enlargement 
of  the  heart,  and  the  effect  of  any  particular  lesion  in  this  respect 
depends  on  the  following  general  considerations : — 

1.  The   valve   affected,    and    the   nature   and   tendency   of   the 

morbid  process  which  is  concerned  in   the  production  of 
the  valvular  defect. 

2.  The  suddenness  and  extent  of  the  lesion. 

3.  The  age,  sex,  occupation,  habits,  and  general  condition  of  the 

patient. 


CHRONIC   ENDOCARDITIS  163 

These  points  will  be  considered  in  detail  under  the  account  of  the 
prognosis  of  valvular  affections. 

Enlargement  of  the  left  side  of  the  heart  is  very  commonly 
accompanied  by  hypertrophy  of  the  right  ventricle,  which,  by 
keeping  up  the  blood  pressure  in  the  pulmonic  circulation,  comes 
to  the  assistance  of  the  left  ventricle. 

Disease  at  any  cardiac  orifice  tends  in  course  of  time  to  produce 
an  increase  in  size  of  the  openings  situated  behind  the  seat  of  the 
lesion.  As  a  rule,  regurgitant  lesions  are  more  effective  in  this 
respect  than  obstructive  disease  in  the  same  situations.  Indeed, 
according  to  Professor  Hamilton,  stenosis  of  the  mitral  or 
aortic  opening  causes  little  or  no  enlargement  of  the  pulmonic 
and  tricuspid  orifices,  but  this  view  is  opposed  to  the  opinion  of 
the  majority  of  writers  on  diseases  of  the  heart.  Nevertheless,  an 
increase  in  size  of  the  pulmonic  opening  is  hardly  ever  observed, 
and  incompetence  of  the  pulmonic  valve  is  one  of  the  rarest  of 
cardiac  lesions. 

EFFECTS  ON  OTHER  ORGANS 

Valvular  disease  of  the  heart  leads,  sooner  or  later,  in  the  large 
majority  of  cases,  to  congestion  of  the  pulmonic  and  systemic 
circulations,  and  is,  in  consequence,  attended  by  disturbance  of 
function  of  the  various  organs  throughout  the  body. 

Moreover,  long-continued  venous  congestion  of  the  viscera  induces 
organic  changes  which  are  most  marked  in  the  lungs,  fiver,  stomach, 
spleen,  kidneys,  brain,  and  heart. 

The  pulmonic  lesions  most  commonly  found  are — congestion  and 
oedema  of  the  lungs,  dilatation  and  rupture  of  the  pulmonic  capil- 
laries, pulmonary  apoplexy,  brown  induration  of  the  lungs,  bronchitis, 
and  lobar  pneumonia. 

In  the  early  stages  of  valvular  disease  the  liver  becomes  enlarged 
and  congested.  Atrophy  and  fatty  degeneration  of  the  hepatic  cells 
ensue,  and  ultimately  the  fibrous  tissue  of  the  organ  is  increased. 
On  section  the  viscus  presents  the  typical  "nutmeg"  appearance. 

The  mucous  membrane  of  the  stomach  and  intestines  is  congested, 
and  may  show  haemorrhages.  Catarrhal  inflammatory  changes  are 
commonly  observed  throughout  the  alimentary  tract. 

The  spleen  is  enlarged  and  firm.  It  shows  on  section  a  dark 
purple  colour  owing  to  congestion.  Infarcts  may  be  seen,  and  the 
fibrous  stroma  of  the  organ  is  increased. 

The  kidneys  are  usually  enlarged  and  indurated.  On  section  the 
medullary  portions  are  seen  to  be  engorged  with  blood,  and  there 
may  be  signs  of  old  or  recent  infarction.  The  kidneys  sometimes 
show  cirrhotic  changes. 

The  vessels  of  the  brain  are  usually  congested,  and  the  organ 
itself  may  be  shrunken.     Signs  of  embolism  may  be  seen. 

The  myocardium   is  not  uncommonly  the  seat  of  pigmentary, 


i64  DISEASES   OF   THE   HEART 

granular,  fatty,  and  fibroid  changes,  with  corresponding  alterations 
in  the  texture  of  the  muscular  substance  of  the  heart. 

The  effects  of  the  above-mentioned  changes  on  the  functional 
activity  of  the  various  organs  act  and  react  on  one  another,  so  that 
a  "  vicious  circle  "  of  events  becomes  established,  which  sooner  or 
later  terminate  in  the  death  of  the  patient. 

Thus  the  interference  with  the  functions  of  secretion  and  ex- 
cretion leads  to  the  imperfect  assimilation  of  food  and  the  accumu- 
lation of  waste  products  in  the  blood,  effects  which  are  aggravated 
by  the  impaired  functional  activity  of  the  nervous  system  and  the 
improper  oxygenation  of  the  blood  in  the  lungs.  Nutrition  is 
thereby  seriously  interfered  with,  and  the  muscular  substance  of  the 
heart  suffers  in  common  with  the  other  tissues.  The  cardiac  mal- 
nutrition leads  to  further  circulatory  embarrassment,  which  in  turn 
aggravates  the  existing  functional  derangement  of  the  organs 
throughout  the  body. 


CHAPTER   X 
CHRONIC   Vy\LVULAR    LESIONS 

Pathogenesis  of  Chronic  Valvular  Disease. 

Under  this  head  it  is  convenient  to  include,  .ill  the  pathological 
processes  which  may  lead  to  an  abnormal  condition  of  any  portion 
of  the  valvular  apparatus  of  the  heart. 

The  causes,  therefore,  of  chronic  valvular  lesions  may  be  classified 
as  follows : — 

1.  Acute  or  sub-acute  endocarditis. — The  lesion  is  usually  on 
the  left  side  of  the  heart,  and  the  mitral  valve  suffers  more  commonly 
than  the  aortic. 

Either  incompetence  of  a  valve  or  obstruction  at  an  orifice  may 
be  produced,  or,  as  usually  happens,  the  two  conditions  are  com- 
bined in  varying  proportions.  The  occurrence  of  obstruction  at  an 
orifice  without  incompetence  of  its  valve  is  a  very  much  rarer  event 
than  that  of  incompetence  of  a  valve  without  obstruction  at  the 
orifice  which  it  guards. 

2.  Chronic  endocarditis  (including  atheroma). — The  lesion  is 
again  most  commonly  situated  on  the  left  side  of  the  heart,  and  in 
cases  of  rheumatic  origin  the  mitral  valve  suffers  more  frequently 
than  the  aortic.  The  aortic  valve  is  usually  the  seat  of  the  chronic 
endocardial  changes  produced  by  strain  and  atheroma. 

Here  again  obstruction  at  an  orifice  is  nearly  always  accompanied 
by  incompetence  of  its  valve.  Incompetence  of  a  valve  sometimes 
occurs  without  obstruction  at  its  aperture,  but  in  the  large  majority 
of  cases  the  two  conditions  are  combined. 

3.  Rupture  of  the  cusp  of  a  valve  or  of  some  of  the  chordae 
tendinese. — This  lesion  may  be  due  to  sudden  muscular  effort,  or 
to  external  violence,  and  is  productive  of  valvular  incompetence. 

4.  Imperfect  coaptation  of  the  curtains  of  a  valve  owing  to 
dilatation  of  the  orifice  which  they  guard. — This  lesion  gives  rise 
to  valvular  incompetence.  Aortic  incompetence  due  to  this  cause 
is  a  very  rare  event,  and  depends  on  a  general  dilatation  of  the  first 
part  of  the  aorta,  involving  the  orifice  of  the  vessel. 

16s 


i66  DISEASES    OF   THE    HEART 

Relative  insufficiency  (as  the  condition  is  usually  termed)  of  the 
pulmonic  valve  is  practically  unknown. 

Mitral  regurgitation  is  not  uncommonly  due  to  dilatation  of  the 
orifice  of  the  valve,  whereby  the  proper  adaptation  of  the  flaps  is 
prevented. 

The  enlargement  of  the  mitral  opening  is,  in  the  large  majority  of 
cases,  part  of  a  general  dilatation  of  the  left  ventricle,  and  the 
muscular  constriction  of  the  orifice,  which  takes  place  during 
systole,  is  insufficient  to  enable  the  valvular  curtains  to  come  into 
apposition.  Defective  muscular  closure  of  the  valve  is  in  some 
instances  the  sole  cause  of  its  insufficiency. 

Tricuspid  incompetence  is,  mutatis  mutandis,  brought  about  in  a 
similar  way. 

5.  Congenital  malformation  of  the  valves  and  intra-uterine 
endocarditis. — Pulmonic  stenosis,  which  is  frequently  associated 
with  some  other  structural  or  valvular  defect  of  the  heart,  is  the 
most  common  congenital  malformation  of  the  cardiac  valves. 

Intra-uterine  endocarditis  usually  affects  the  right  side  of  the 
heart,  and  the  pulmonic  valve  suffers  more  frequently  than  the 
tricuspid. 


CHAPTER   XI 
MITRAL    INCOMPETENCE 


Pathogenesis  —  Morbid  anatomy  —  Compensation  :  its  method  of  production 
and  maintenance  ^Failure  of  compensation,  and  its  results — Symptoms  — 
Complications  —  Physical  signs  —  Diagnosis — Estimation  of  the  amount  of 
regurgitation. 

ETIOLOGICAL   PATHOLOGY 

Under  normal  conditions  the  complete  apposition  of  the  two 
segments  of  the  mitral  valve  during  the  ventricular  systole,  whereon 
the  closure  of  the  opening  depends,  is  obtained  by  means  of  (a)  the 
narrowing  of  the  aperture  that  is  produced  by  the  contraction  of 
the  muscular  fibres  surrounding  it,  and  (^)  the  contraction  of  the 
musculi  papillares,  which,  through  the  chordae  tendinese,  draws 
down  and  approximates  the  curtains  of  the  valve,  and  at  the  same 
time  prevents  their  eversion  into  the  auricle.  Imperfect  closure  of 
the  mitral  orifice,  and  consequently  leakage  into  the  left  auricle  during 
the  ventricular  systole,  may  be  due  to  any  cause  which  interferes  with 
the  accurate  apposition  of  the  curtains  of  the  valve.  Thus  it  may 
depend  on  (a)  structural  disease  in  any  portion  of  the  valvular 
apparatus,  (d)  enfeeblement  of  the  muscular  structures  concerned 
in  the  efficient  working  of  the  valve,  and  (c)  defective  co-ordination 
of  the  series  of  events  which  determine  the  perfect  action  of  the 
valvular  mechanism.  As  a  consequence  of  acute  or  chronic  endo- 
carditis the  free  edges  of  the  curtains  of  the  valve  may  become 
thickened,  retracted,  ulcerated,  or  otherwise  deformed,  so  that  the 
adequate  apposition  of  the  cusps  is  rendered  impossible.  In  other 
instances  the  flaps  are  perforated,  or  they  become  adherent  to  one 
another,  or  to  the  walls  of  the  heart,  or  their  proper  adaptation  is 
prevented  by  a  growth  of  vegetations. 

The  valvular  inadequacy  depends,  in  some  cases,  on  atheromatous 
changes,  which  most  commonly  attack  the  large  anterior  segment 
of  the  valve,  and  may  lead  to  softening,  ulceration,  or  calcification 
of  this  structure. 

The  chordae  tendineae  may  be  thickened,  rigid,  or  shortened, 
but,  on  the  other  hand,  they  sometimes  become  stretched,  and 
occasionally  rupture.  The  papillary  muscles  frequently  show 
degenerative  changes,  and  in  some  instances  the  muscle  fibres  are 
more  or  less  replaced  by  fibrous  tissue. 

The  rupture  of  a  cusp,  or  of  one  or  other  of  the  chordse  tendinese, 

167 


i68  DISEASES  OF  THE  HEART 

or  musculi  papillares,  is,  in  occasional  instances,  the  cause  of  mitral 
insufficiency. 

Regurgitation  through  the  mitral  orifice  is  very  commonly  due  to 
relative  or  muscular  incompetence  of  the  valve. 

The  two  conditions  are  usually  combined,  and  are  the  result  of 
dilatation  of  the  left  ventricle  from  long-continued  strain  (such  as 
accompanies  protracted  high  arterial  tension,  aortic  valvular  disease, 
etc).,  and  of  muscular  enfeeblement,  consequent  on  -aneemia,  pro- 
longed fevers,  myocarditis,  and  malnutrition,  or  degeneration  of  the 
myocardium  from  any  cause. 

The  incompetence  of  the  mitral  valve  that  not  infrequently  arises 
during  middle  life  and  old  age  is  due  to  one  or  other  of  these  causes 
acting  singly  or  in  combination.' 

The  valvular  incompetence  depends  on  the  inability  of  the 
segments  of  the  valve  to  come  into  complete  apposition,  in  con- 
sequence either  of  the  increase  in  the  size  of  the  mitral  orifice 
which  accompanies  dilatation  of  the  left  ventricle  (relative  incom- 
petence), or  of  the  insufficient  constriction  of  the  opening  by  its 
enfeebled  muscular  sphincter  during  the  ventricular  systole  (muscular 
incompetence). 

It  is  obvious,  however,  that  relative  incompetence  must  necessarily 
be  accompanied  by  muscular  inadequacy,  whereas  muscular  inade- 
quacy, sufficient  to  give  rise  to  valvular  incompetence,  might  exist 
without  producing  any  dilatation  of  the  opening ;  but,  as  previously 
mentioned,  the  two  conditions  are  almost  always  combined. 

PATHOLOGICAL   RESULTS 
The  Effects  on  the  Heart  and  Circulation 

In  consequence  of  the  incomplete  shutting  of  the  mitral  valve, 
blood  is  forced  backwards  into  the  left  auricle  during  the  ventricular 
contraction.  The  auricle,  therefore,  now  receives  blood  from  two 
sources,  i.e.  from  the  pulmonic  veins,  and  from  the  left  ventricle, 
and  at  the  end  of  its  diastole  its  contents  exceed  the  normal  by  the 
amount  which  has  regurgitated  from  the  ventricle. 

The  accommodation  of  this  increased  quantity  of  blood  involves 
dilatation  of  the  auricle  from  overfilling.  The  auricular  walls  sub- 
sequently hypertrophy,  in  consequence  of  the  additional  work  entailed 
by  the  propulsion  into  the  left  ventricle  of  a  greater  amount  of 
blood  than  usual ;  but  owing  to  the  nature  of  the  lesion  and  the 
thinness  of  the  muscular  covering  of  the  auricle,  dilatation  is  always 
in  excess  of  hypertrophy. 

The  abnormal  strain  to  which  the  walls  of  the  auricle  are  subjected 
usually  gives  rise  also  to  more  or  less  thickening  of  the  endocardium 
lining  the  cavity. 

Owing  to  the  increase  in  the  auricular  contents,  blood  is  propelled 
in  larger  quantity,  and  with  greater  force  than  usual,  into  the  left 


MITRAL  INCOMPETENCE  169 

ventricle  during  diastole,  so  that  dilatation  of  the  chamber  from 
overfilling  is  produced.  Hypertrophy  also  occurs  as  the  result  of 
the  increased  work  involved  in  the  expulsion  of  the  unusually  large 
volume  of  blood  contained  in  the  ventricle  and  in  the  maintenance 
of  the  tone  of  the  ventricular  wall. 

The  high  pressure  which  prevails  in  the  left  auricle,  especially 
during  the  ventricular  systole,  is  felt  also  in  the  pulmonic  veins  and 
capillaries,  and  gives  rise  to  interference  with  the  outward  flow  of 
blood  in  these  vessels.  The  obstruction  to  the  free  passage  of  blood 
through  the  lungs,  thus  induced,  is  followed  by  a  general  rise  of 
pressure  in  the  pulmonic  circulation  by  reason  of  the  more  vigorous 
action  of  the  right  ventricle  in  the  face  of  the  additional  work  that 
is  required  of  it.  Under  favourable  circumstances  the  increased 
functional  activity  of  the  ventricle  results  in  hypertrophy  of  its 
walls,  which  is  essentially  a  conservative  process,  since,  by  maintain- 
ing a  high  blood  pressure  in  the  pulmonic  circuit  and  left  auricle, 
it  lessens  the  regurgitation  through  the  mitral  opening,  and  thereby 
increases  the  quantity  of  blood  supplied  to  the  aorta. 

Long-continued  high  tension  in  the  pulmonic  circulation  gives  rise, 
sooner  or  later,  to  more  or  less  thickening,  congestion,  and  dilata- 
tion of  the  pulmonic  vessels,  with  fibrotic  induration  of  the  lungs. 

The  condition  known  as  "brown  induration"  of  the  lungs  re- 
presents these  changes  in  an  advanced  stage. 

It  will  be  observed  that  compensation  in  cases  of  mitral  regurgi- 
tation is  effected  chiefly  by  means  of  hypertrophy  of  the  right 
ventricle.  The  hypertrophy  of  the  left  auricle  is  insufficient  to  be 
of  much  practical  service.  Dilatation  of  the  left  ventricle,  if  com- 
bined with  adequate  hypertrophy,  is  beneficial  in  so  far  as  the 
increased  capacity  of  the  chamber  neutralizes,  to  some  extent  at 
least,  the  amount  of  back-flow ;  but  the  powerful  systole,  while 
augmenting  the  blood  supply  to  the  aorta,  also  aggravates  the  leak- 
age through  the  mitral  opening,  and  in  this  respect  is  harmful. 

The  development,  maintenance,  and  duration  of  the  compensatory 
changes  depend  on  the  following  considerations  : — 

1.  The  quality  and  quantity  of  the  blood  supplied  to  the  myo- 

cardium. 

2.  The  suddenness,  extent,  and  tendency  of  the  valvular  lesion. 

3.  The   recuperative   power   and   endurance   of    the    patient   as 

evidenced  by  his  age,   family  history,   habits,  general  con- 
dition, and  so  forth. 

4.  The  presence  or  absence  of  complications. 

Incompetence  of  the  mitral  valve,  slowly  developed,  of  moderate 
severity,  and  stationary  in  character,  occurring  in  a  young  and  other- 
wise healthy  adult,  may,  in  the  absence  of  complications,  give  rise 
to  compensatory  changes  which  endure  for  years,  and  more  or  less 
completely  restore  the  normal  balance  of  the  circulation. 


1.70  DISEASES   OF   THE   HEART 

In  the  majority  of  cases,  however,  compensation  is  less  perfect, 
with  the  result  that  a  diminished  supply  of  blood  to  the  aorta  and 
systemic  vessels  leads  to  arterial  ansemia,  accompanied  by  con- 
gestion in  the  pulmonic  area,  and  later  by  a  varying  degree  of 
general  venous  plethora. 

Failure  of  compensation  is  usually  slowly  developed,  in  conse- 
quence either  of  the  progressive  character  of  the  lesion,  or  of  the 
gradual  enfeeblement  of  the  muscular  power  of  the  ventricles, 
induced  by  long-continued  overwork.  The  ordinary  sequence  of 
events  characteristic  of  cardiac  failure  may,  however,  be  interrupted 
at  any  stage  of  the  process  by  the  occurrence  of  pulmonic  or  other 
complications,  which,  not  infrequently,  give  rise  to  acute  dilatation 
of  the  heart. 

Lung  affections,  especially  bronchitis,  pneumonia,  pleurisy  with 
effusion,  etc.,  and  intercurrent  attacks  of  pericarditis  or  endocarditis, 
are  a  fertile  source  of  failure  of  the  right  ventricle,  owing  to  the 
additional  strain  thereby  thrown  on  the  already  overtaxed  walls  of 
this  chamber. 

In  whatever  manner  produced,  failure  of  compensation  is  charac- 
terised by  a  series  of  further  changes,  which,  unless  capable  of 
removal,  terminate  in  the  death  of  the  patient. 

Owing  either  to  the  absolute  or  relative  weakness  of  its  muscular 
walls,  the  right  ventricle  fails  to  completely  discharge  its  contents 
at  each  systole,  and  in  consequence  undergoes  gradual  dilatation 
from  incomplete  emptying.  Coincidently  with  this  process,  muscular 
and  relative  incompetence  of  the  tricuspid  valve  is  established.  The 
blood  supply  to  the  right  auricle  now  exceeds  the  normal  by  the 
amount  which  escapes  backwards,  with  each  systole,  through  the 
tricuspid  valve ;  consequently  the  chamber  undergoes  dilatation 
from  overfilling.  Hypertrophy  of  the  auricular  walls  may  ensue, 
but  this  is  seldom  well  marked,  and  from  anatomical  considerations 
alone  can  be  of  little  practical  value.  Further  dilatation  of  the  right 
auricle  from  incomplete  emptying  quickly  supervenes,  and  is  accom- 
panied by  congestion  and  engorgement  of  the  venae  cavee  and 
vessels  of  the  portal  and  systemic  venous  S5'Stems. 

Moreover,  the  establishment  of  tricuspid  incompetence  must 
necessarily  be  followed  by  a  fall  of  blood  pressure  in  the  pulmonic 
circulation  and  left  auricle,  the  effect  of  which  is  to  still  further 
increase  the  leakage  through  the  mitral  orifice,  and  thereby  add 
to  the  embarrassment  of  the  right  ventricle,  in  addition  to  diminish- 
ing the  supply  of  blood  to  the  aorta. 

It  will  thus  appear  that  failure  of  compensation  in  cases  of  mitral 
disease  results  in  the  establishment  of  a  train  of  events,  which  act 
and  react  injuriously  on  one  another,  and  tend  to  the  production 
of  arterial  anaemia,  accompanied  by  ever-increasing  pulmonic  and 
systemic  venous  engorgement. 

The  effects  of  this  "back-working"  process  on  the  functional 
activity   and    structural   arrangements   of   the   heart,    lungs,    brain, 


MITRAL   INCOMPETENCE  171 

liver,  and  other  abdominal  organs  have  already  (see  p.  163)  been 
described,  and  need  not  be  recapitulated.  Dropsy  due  to  cardiac 
causes  first  manifests  itself  in  those  parts  furthest  away  from  the 
heart,  where  presumably  the  circulation  is  most  feeble.  It  com- 
mences, therefore,  in  the  feet,  and  gradually  spreads  upwards,  and 
may  ultimately  involve  all  the  subcutaneous  tissues.  Effusion  into 
the  serous  cavities  of  the  abdomen,  pleurae,  pericardium,  etc., 
also  occurs,  and  collections  of  fluid,  even  when  small  in  amount, 
in  any  of  these  situations  are  always  a  source  of  serious  cardiac 
embarrassment. 


SYMPTOMS 

In  all  forms  of  chronic  valvular  disease  of  the  heart  the  occurrence 
of  symptoms  and  the  severity  of  their  manifestation  are  determined, 
for  the  most  part,  by  the  degree  of  adequacy  of  the  compensatory 
changes.  The  more  perfect  the  compensation,  or,  in  other  words, 
the  more  nearly  the  normal  balance  between  the  arterial  and 
venous  circulations  is  restored,  the  fewer  and  less  important  are 
the  symptoms. 

In  some  instances  compensation  is  so  complete  that  the  patient 
is  not  aware  that  he  is  the  subject  of  heart  disease,  but  in  the 
majority  of  cases  it  is  less  adequate,  and  sooner  or  later  the 
symptoms  and  signs  of  cardiac  insufficiency  make  their  appearance. 
The  period  of  occurrence  and  the  character  of  the  symptoms  are 
by  no  means  constant  for  any  given  lesion,  and  they  vary  greatly 
in  different  forms  of  valvular  disease,  but  in  all  cases  they  are 
referable  to  mechanical  disturbance  of  the  systemic  and  pulmonic 
circulations,  or  to  disordered  action  of  the  heart. 

In  fully  compensated  cases  regurgitation  through  the  mitral  orifice 
may  give  rise  to  no  symptoms,  but  as  a  rule  patients  suffering  from 
this  disease  complain  of  shortness  of  breath  when  any  unusual 
effort  is  made.  The  liability  to  dyspnoea  on  exertion,  which  is 
common  to  all  forms  of  compensated  valvular  disease,  is  much 
more  marked  in  the  early  stages  of  mitral  than  of  aortic  affections. 
The  reason  is  that  lesions  of  the  mitral  valve  must,  from  the  outset, 
lead  to  a  rise  of  pressure  in  the  pulmonic  circulation,  whereas  aortic 
disease,  in  its  early  stages,  has  little  or  no  influence  in  this  respect. 
As  compensation  begins  to  fail  the  dyspnoea  becomes  more  pro- 
nounced and  more  easily  excited,  and  is  often  associated  with 
cough,  which  is  sometimes  dry  and  irritable,  while  at  others  it  is 
attended  by  a  profuse  watery  expectoration. 

Attacks  of  palpitation,  accompanied  by  irregularity  of  the  heart, 
and  prjecordial  uneasiness,  or  pain,  may  be  of  frequent  occurrence, 
and  may  arise  on  very  slight  provocation. 

In  some  instances  the  patient  first  comes  under  observation 
complaining  of  dyspepsia,   flatulence,   and  irregular  action  of  the 


172  DISEASES    OF   THE    HEART 

bowels,  or  it  may  happen  that  cedema  of  the  feet  and  legs  is  the 
earliest  indication  of  the  cardiac  insufficiency. 

In  any  event  shortness  of  breath  soon  becomes  a  troublesome 
and  prominent  symptom,  and  is  quickly  followed  by  evidence  of 
congestion  of  the  lungs  and  other  viscera. 

The  effects  of  venous  engorgement  of  these  organs  are  the  same 
for  all  forms  of  valvular  disease,  and  since  they  are  so  marked  in 
mitral  lesions,  and  especially  in  mitral  regurgitation,  a  general 
account  of  the  symptoms  arising  therefrom  will  be  given  in  this 
place. 

Pulmonic. — The  earliest  and  most  important  indication  of  pul- 
monic congestion  is  dyspnoea,  which  gradually  increases  in  severity 
as  the  cardiac  failure  becomes  more  pronounced.  In  the  final 
stages  of  the  disease  the  difficulty  in  breathing  frequently  takes 
the  form  of  orthopncea. 

Paroxysmal  attacks  of  dyspnoea  of  an  asthmatic  nature  are  by 
no  means  rare  in  the  course  of  mitral  affections. 

Cough  is  often  very  troublesome,  and  hjemoptysis  sometimes 
occurs  in  consequence  of  the  rupture  of  a  vessel  in  the  lungs. 

Examination  of  the  lungs  reveals  the  presence  of  oedema  of  the 
bases  and  dependent  parts,  and  not  uncommonly  the  signs  of 
bronchitis. 

Hydrothorax  may  occur  as  part  of  a  general  dropsy,  or  as  the 
result  of  an  acute  inflammation  of  the  pleural  membrane. 

Epistaxis  is  not  uncommon,  and  may  give  rise  to  serious  loss  of 
blood. 

Portal. — Enlargement  of  the  liver,  with  tenderness  of  the  organ, 
is  one  of  the  earliest  indications  of  interference  with  the  flow  of 
blood  through  the  right  heart. 

Gastro-intestinal  congestion  is  attended  by  loss  of  appetite, 
nausea,  dyspepsia,  flatulence,  and  irregular  action  of  the  bowels. 
Haematemesis  and  melsena  sometimes  occur,  and  haemorrhoids 
may  be  a  source  of  great  discomfort. 

Genito- Urinary. — Renal  congestion  is  shown  by  a  diminished 
secretion  of  urine,  which  is  high-coloured,  and  throws  down,  on 
cooling,  a  copious  deposit  of  lithates.  Albumen  is  usually  present 
in  small  quantities.  Casts  are  not  found  in  the  absence  of  structural 
disease  of  the  kidneys. 

Uterine  congestion  is  accompanied  by  disorders  of  menstruation 
and  occasionally  by  menorrhagia. 

Cerebral. — Headache,  giddiness,  faintness,  vertigo,  and  especially 
sleeplessness,  are  associated  with  the  congestion  of  the  circulation 
through  the  brain.  Delirium  sometimes  occurs,  and  is  of  grave 
import.  Cheyne-Stokes'  respiration  occasionally  attends  the  final 
stages  of  failure  of  the  heart. 


MITRAL    INCOMPETENCE  173 

Cutaneous. — The  patient  commonly  presents  an  ansemic  appear- 
ance, while  the  skin  has  often  a  dirty  yellow  tinge.  The  con- 
junctivse  are  pale.  Cyanosis  of  the  Hps,  face,  and  extremities  is 
frequently  observed,  though,  on  the  other  hand,  in  not  a  few 
instances  a  condition  of  extreme  pallor  is  found  in  these  situations. 

The  patient  loses  flesh,  and  this  is  especially  noticeable  in  the 
case  of  children. 

Dropsy  begins  with  swelling  of  the  ankles,  and  gradually  spreads 
upwards.  It  may  involve  the  serous  cavities.  Thrombosis  in  the 
large  venous  trunks  may  lead  to  a  peculiarly  solid  form  of  oedema 
in  the  area  drained  by  the  vessel  that  is  affected.  The  swollen  sub- 
cutaneous tissues  may  be  the  seat  of  erysipelatous  inflammation,  or 
even  of  gangrene. 

Haemorrhages  into  the  skin  are  not  uncommon,  but  they  are 
usually  very  small. 

Failure  of  compensation  may  be  recovered  from,  and  its  effects 
removed  by  means  of  suitable  treatment,  but  each  attack  leaves 
the  heart  and  tissues  more  or  less  crippled  and  less  capable  of 
resisting  the  further  inroads  of  the  disease. 

As  a  rule  death,  in  cases  of  mitral  incompetence,  takes  place 
slowly,  and  depends  on  gradual  enfeeblement  and  dilatation  of  the 
ventricles,  and  especially  of  the  right,  since  it  is  on  this  chamber 
that  the  stress  of  the  lesion  mainly  falls. 

Sudden  death  in  mitral  regurgitation  is  of  comparatively  rare 
occurrence,  but  it  may  happen  as  the  result  of  embolism  or  cerebral 
haemorrhage. 


COMPLICATIONS 

The  commonest  and  most  important  complications  of  mitral  re- 
gurgitation are  those  affecting  the  lungs.  Acute  bronchitis,  pulmonic 
oedema,  pleurisy  with  effusion,  pneumonia,  etc.,  may  at  any  period 
of  the  disease  give  rise  to  urgent  cardiac  symptoms  by  reason  of 
the  additional  strain  thereby  imposed  on  the  right  ventricle. 

Extensive  dropsy  and  especially  effusion  into  the  pericardial, 
pleural,  or  peritoneal  cavity,  add  greatly  to  the  embarrassment  of 
the  heart. 

Embolic  manifestations  may  appear  at  any  stage  of  the  disease. 
The  spleen,  kidneys,  brain,  and  skin  are  the  organs  most  commonly 
affected. 

Thrombosis  sometimes  occurs  in  the  large  venous  trunks,  and 
may  give  rise  to  various  symptoms. 

Severe  cardiac  pain  is  occasionally  associated  with  mitral  in- 
competence, but  it  very  rarely  happens  that  an  attack  of  angina 
pectoris  is  experienced. 

Pericarditis  is  not  an  uncommon  complication  of  mitral  disease, 
and  is  more  frequently  observed  in  children  than  in  adults. 


174  DISEASES   OF   THE   HEART 


PHYSICAL  SIGNS 

Physiognomy. — The  observation  of  the  physiognomy  in  cases  of 
morbus  cordis  forms  an  important  part  of  the  physical  examination, 
and  often  furnishes  valuable  indications  of  the  nature  and  severity 
of  the  lesion. 

Attention  should  be  directed  mainly  to  the  following  points,  viz. 
the  expression,  complexion,  colour  of  the  skin,  attitude,  conforma- 
tion, state  of  nutrition,  and  general  appearance  of  the  patient. 

The  face  in  mitral  regurgitation  often  appears  somewhat  suffused 
and  puffy,  and  is  frequently  the  seat  of  venous  stigmata,  scattered 
about  either  singly  or  in  clusters.  There  is  commonly  more  or 
less  cyanosis  of  the  lips,  cheeks,  ears,  nose,  and  extremities,  though 
in  some  instances  the  complexion  is  of  an  ashy  grey  hue.  The 
conjunctivae  and  skin,  with  the  exception  of  the  parts  above- 
mentioned,  are  usually  anaemic,  and  in  the  late  stages  of  the  disease 
frequently  present  a  dirty  yellow  discolouration,  in  consequence,  no 
doubt,  of  the  continued  congestion  of  the  liver. 

The  attitude  of  the  patient  is  often  highly  suggestive.  Thus  there 
may  be  orthopnoea,  or  the  position  assumed  may  be  such  that  the 
accessory  muscles  of  respiration  can  be  most  advantageously  brought 
into  play. 

Clubbing  of  the  fingers  is  sometimes  observed  in  old-standing 
cases  of  mitral  incompetence. 

The  muscles  become  soft  and  flabby,  and  loss  of  flesh  is  by  no 
means  uncommon.  The  emaciation  may  be  masked  by  dropsy  of 
the  subcutaneous  tissues,  especially  in  the  terminal  stages  of  the 
disease. 

Pulse. — During  the  period  of  compensation  the  pulse  is,  as  a  rule, 
fairly  regular  in  frequency,  but  irregular  in  force.  The  artery  is 
of  medium  size,  and  cannot  usually  be  felt  betw^een  the  beats.  The 
pulse  wave  is  short,  badly  sustained,  and  easily  compressible.  With 
the  appearance  of  symptoms  the  pulse  rate  is  increased,  and  the 
beats  become  markedly  irregular  both  in  force  and  frequency.  The 
pulse  wave  grows  shorter,  less  sustained,  and  more  easily  obliterated 
by  pressure  with  the  finger,  and  the  vessel  is  empty  between  the 
beats.  Speaking  generally,  the  pulse  of  mitral  regurgitation  is 
characterized  by  irregularity  as  regards  both  force  and  frequency, 
and  also  by  low  tension.  For  further  information  the  reader  is 
referred  to  the  section  dealing  with  the  pulse. 

HEART 

Inspection. — Bulging  of  the  prscordium  is  sometimes  observed 
in  young  subjects,  with  yielding  chest  walls. 

The  apex  beat  of  the  heart  is  displaced  outwards  and  slightly 


MITRAL   INCOMPETENCE  irS 

downwards.  The  outward  displacement  is  due  partly  to  the  dilata- 
tion of  the  left  ventricle  and  partly  to  the  enlargement  of  the  right 
heart,  which  tends  to  tilt  the  apex  outwards.  The  downward  dis- 
placement of  the  apex  beat  is  due  to  the  hypertrophy  of  the  left 
ventricle.  Epigastric  pulsation  is  often  well  marked,  in  consequence 
of  the  forcible  contraction  of  the  hypertrophied  right  ventricle. 

Palpation.  — The  impulse  of  the  heart  is  diffused  and  forcible,  and 
is  usually  best  appreciated  over  the  right  ventricle  and  in  the  epi- 
gastrium. 

A  thrill,  systolic  in  time,  can  sometimes  be  felt  at  the  apex. 

Percussion. — The  area  of  cardiac  dulness  is  increased  chiefly  in  a 
lateral  direction,  and  to  the  right  more  than  to  the  left.  The  reason 
for  this  is  obvious.  The  upper  limit  of  dulness  is  slightly  raised  in 
consequence  of  the  enlargement  of  the  left  auricle. 

Auscultation. — At  the  apex  the  first  sound  is  accompanied  by  a 
blowing  systolic  murmur,  which  is  transmitted  outwards  into  the  left 
axilla,  and  not  infrequently  backwards,  as  far  as  the  angle  of  the 
left  scapula. 

The  murmur  is  sometimes  propagated  upwards  and  inwards,  and 
may  be  audible  along  the  left  sternal  edge  as  high  as  the  third  or 
second  rib.  It  occasionally  happens  that  the  murmur  can  be  heard 
over  the  whole  prsecordium,  and  in  exceptional  instances  over  the 
whole  thorax. 

The  murmur  is  usually  loudest  at  the  apex,  and  gradually  "tails 
off"  as  the  stethoscope  passes  into  the  axilla  on  the  one  hand,  or 
towards  the  sternum  on  the  other. 

In  rare  instances  the  loudness  of  the  bruit  is  most  marked  over 
the  second  left  interspace  and  adjoining  ribs,  close  to  the  sternum. 
The  phenomenon  is  supposed  to  depend  on  the  nearer  approach 
than  usual  of  the  enlarged  left  auricle  to  the  chest  wall,  in  conse- 
quence of  the  retraction  of  the  left  lung. 

The  systolic  murmur  heard  at  the  apex  may  partially  or  wholly 
obscure  the  first  sound,  or  may  follow  it. 

At  the  base  of  the  heart  the  sounds  over  the  aortic  cartilage  are 
unchanged,  but  over  the  pulmonic  cartilage  the  second  sound  is 
accentuated.  Reduplication  of  the  second  sound  is  often  observed 
over  the  base  of  the  heart.  When  the  right  ventricle  fails,  and  tri- 
cuspid incompetence  is  established,  the  accentuation  of  the  pulmonic 
second  sound  is  lost  owing  to  the  fall  of  blood  pressure  in  the  lungs. 
A  systolic  murmur  due  to  tricuspid  regurgitation  may  become 
audible  over  the  ensiform  cartilage  and  base  of  the  sternum.  The 
concurrent  signs  of  tricuspid  incompetence  are  distension  and  occa- 
sional pulsation  of  the  veins  in  the  neck,  enlargement  of  the  liver, 
and  congestion  of  the  portal  and  systemic  venous  circulations, 
together  with  its  effects.  Hepatic  pulsation  is  also  sometimes 
observed. 


176  DISEASES    OF   THE    HEART 


DIAGNOSIS 

The  diagnosis  of  mitral  regurgitation  rests  mainly  on  the  presence 
of  a  systolic  bruit  at  and  to  the  left  of  the  apex,  in  association 
with  accentuation  of  the  pulmonic  second  sound,  and  the  signs 
of  enlargement  of  the  right  ventricle.  It  sometimes  happens  that 
the  murmur  is  absent,  or  inaudible,  as,  for  instance,  when  the 
ventricular  contractions  are  either  very  feeble  or  extremely  rapid. 
Under  these  circumstances  the  diagnosis,  which  is  seldom  a  matter 
of  much  doubt,  must  be  based  on  the  concomitant  signs  and 
symptoms  of  pulmonic  and  systemic  venous  engorgement,  and- 
of  dilatation  of  the  left  and  right  sides  of  the  heart. 

A  systolic  murmur  in  the  mitral  area  is  sometimes  of  exocardial 
origin,  and  may  depend  on  disease  of  the  pericardium,  pleurse,  or 
lungs.  The  differential  diagnosis  of  exo-  and  endocardial  bruits 
has  already  been  considered  (see  p.  70),  and  seldom  presents  much 
difficulty  in  adults. 

In  children,  however,  a  systolic  exocardial  murmur  at  the  apex 
due  to  pericarditis  may  closely  simulate  the  bruit  of  mitral  regurgi- 
tation. The  difficulty  of  differentiating  between  the  two  is  in- 
creased by  the  fact  that  relative  incompetence  of  the  mitral  valve 
not  uncommonly  depends  on  the  myocarditis  that  so  frequently 
accompanies  pericardial  inflammation. 

Systolic  murmurs  produced  at  the  aortic,  pulmonic,  and  tri- 
cuspid orifices  are  sometimes  audible  at  the  apex,  but  their  site 
of  maximum  intensity,  and  the  direction  of  their  transmission, 
taken  in  conjunction  with  the  condition  of  the  right  and  left  sides 
of  the  heart,  and  the  characters  of  the  pulse,  usually  suffice  to 
distinguish  them  from  mitral  bruits. 

If  these  sources  of  error  can  be  excluded,  and  the  diagnosis 
of  mitral  regurgitation  is  thereby  established,  the  cause  of  the 
valvular  insufficiency  still  remains  to  be  considered. 

Regurgitation  through  the  mitral  orifice  may  depend  on  (a) 
organic  disease  of  some  portion  of  the  valvular  apparatus,  or  (/5) 
muscular  relaxation  of  the  opening  whereby  the  segments  of  the 
valve  are  unable  to  come  into  complete  apposition  during  systole. 

The  differential  diagnosis  is  a  matter  of  considerable  importance 
from  the  point  of  view  of  treatment,  inasmuch  as  the  latter  con- 
dition is  curable,  while  the  former  is  not. 

The  two  morbid  processes  sometimes  co-operate  in  the  pro- 
duction of  mitral  incompetence,  and  it  is  then  practically  impossible 
to  estimate  their  relative  influence  and  importance. 

In  practice  it  is  found  that  the  difficulty  in  distinguishing  the 
cause  of  mitral  insufficiency  arises  most  commonly  in  connection 
with  the  appearance  of  an  apical  systolic  murmur  in  association  with 
anaemia,  or  during  the  course  of  an  acute  febrile  disorder. 

The  reason  for  this  is  that  while  angemia  and  acute  febrile  dis' 


MITRAL    INCOMPETENCE  I77 

orders  are  prolific  sources  of  muscular  incompetence  of  the  mitral 
valve,  they  are  also  associated,  either  directly  or  indirectly,  with  the 
conditions  under  which  organic  valvular  disease  may  arise. 

Thus  the  differential  diagnosis  of  mitral  incompetence  which  is 
observed  in  a  patient  who  presents  a  definite  rheumatic  history, 
and  is  also  the  subject  of  well-marked  ansemia,  or  who  is  suffering 
from  acute  rheumatism,  scarlet  fever,  or  measles,  etc.,  may  give  rise 
to  considerable  difficulty.  _  » 

The  recognition  of  the  cause  of  the  mitral  insufficiency  in  cases  \ 
of  this  kind  rests,  for  the  most  part,  on  the  history  and  general  ^ 
condition  of   the  patient,   taken  in  conjunction  with  the  cardiac  | 

physical  signs. 

For  instance,  in  the  case  of  a  patient  suffering  from  ansemia,  the 
differential  diagnosis  of  incompetence  of  the  mitral  valve  depends 
on  the  following  considerations  : — 

1.  T/ie  history  and  general  condition  of  the  patient. — A  history 
of  acute  rheumatism  would  be  evidence  in  favour  of  organic 
disease  of  the  mitral  valve.  On  the  other  hand,  well-marked 
pallor  of  the  skin  and  mucous  membranes,  with  no  emaciation, 
and  the  absence  of  the  signs  of  congestion  in  the  pulmonic  and 
systemic  venous  circulations,  would  point  to  incompetence  of  the 
valve  from  myocardial  enfeeblement. 

2.  The  condition  of  the  hea.rt  ajid  the  characters  of  the  murmur, 
pulmonic  second  soutid,   and  pulse. — In  ansemia   the   apex   beat  is 
seldom  displaced  to  any  great  extent,  the  ventricular  systole  is  not . 
forcible,  and  the  signs  of  cardiac  enlargement,  when  present,  are 
those  of  dilatation,  and  not  of  hypertrophy. 

Generally  speaking,  a  murmur  due  to  muscular  incompetence 
of  the  mitral  valve  follows,  and  does  not  replace,  the  first  sound 
of  the  heart.  Moreover,  the  bruit  is  usually  soft  and  blowing  in 
character;  it  is  not  well  conducted,  and  is  seldom  heard  in  the 
left  axilla,  or  at  the  angle  of  the  left  scapula.  Furthermore,  a 
murmur  at  the  apex,  due  to  ansemia,  is  almost  invariably  preceded 
and  accompanied  by  a  venous  hum  in  the  neck,  and  a  pulmonic 
systolic  bruit. 

Accentuation  of  the  pulmonic  second  sound  is  rarely  well  marked 
in  the  absence  of  organic  disease. 

The  tension  of  the  pulse  is  increased  in  many  cases  of  ansemia, 
especially  in  the  early  stages  of  the  disorder,  and  this  is  never 
observed  in  organic  disease  of  the  heart  productive  of  incompetence 
of  the  mitral  valve. 

3.  The  effects  of  treatment. — Cardiac  murmurs,  due  to  ansemia, 
disappear  under  the  administration  of  hsematinics,  so  soon  as  the 
blood  is  restored  to  its  normal  condition,  and  the  healthy  nutrition 
of  the  cardiac  muscle  is  re-established. 

The  diagnosis  of  the  cause  of  the  mitral  insufficiency  which  is 
frequently  observed  during  the  course  of  an  acute  febrile  disorder, 

N 


1/8  DISEASES   OF   THE    HEART 

such  as  acute  rheumatism,  enteric  fever,  measles,  etc.,  has  already  been 
considered  under  the  head  of  "Acute  Endocarditis"  (see  p.  146). 

It  turns  on  the  period  of  the  attack  at  which  the  apical  systolic 
murmur  is  developed,  and  on  the  presence  or  absence  of  the  signs 
and  symptoms  of  mechanical  disturbance  of  the  circulation.  In 
many  instances,  however,  the  solution  of  the  problem  is  impossible 
until  some  time  has  elapsed  after  the  subsidence  of  the  acute  process. 

The  differentiation  of  the  cause  of  the  incompetence  of  the  mitral 
valve,  which  is  commonly  associated  wkh  chorea,  is  based  on 
considerations  similar  to  those  already  indicated. 

In  exophthalmic  goitre,  again,  a  like  method  of  reasoning  is 
applicable. 

The  muscular  and  relative  incompetence  of  the  mitral  valve 
which  attends  dilatation  of  the  left  ventricle  from  long-continued 
strain  in  cases  of  aortic  disease  and  protracted  high  arterial  tension 
hardly  come  within  the  scope  of  the  present  discussion,  and  are 
considered  elsewhere. 

Prolonged  high  arterial  tension  is  a  cause  both  of  organic  valvular 
disease  and  of  myocardial  overwork,  hence  it  plays  an  important 
role  in  the  production  of  mitral  insufficiency.  In  cases  of  this  kind 
it  is  almost  impossible  to  determine  whether  the  valvular  incom- 
petence is  due  to  organic  disease,  or  to  muscular  enfeeblement,  or 
to  a  combination  of  these  conditions. 

A  similar  difficulty  is  frequently  experienced  in  the  differential 
diagnosis  of  the  mitral  insufficiericy  which  comes  on  inijidiotisiy 
during  and  after  middle  age. 


THE  ESTIMATION  OF  THE  AMOUNT  OF 
REGURGITATION   IN  MITRAL  INCOMPETENCE 

The  estimation  of  the  extent  of  the  valvular  lesion,  or  rather 
of  the  amount  of  blood  which  regurgitates  into  the  left  auricle 
during  each  systole,  is  based  on  the  information  derived  from  the 
following  sources : — 

I.  The  characters  of  the  pulse. — Attention  in  this  respect  should 
be  directed  chiefly  to  the  size  and  strength  of  the  pulse  and  to  the 
condition  of  the  artery  between  the  beats. 

A  small,  weak  and  short  pulse  of  low  tension,  associated  with  a 
forcible  ventricular  contraction,  is,  for  obvious  reasons,  indicative  of 
a  considerable  amount  of  regurgitation.  On  the  other  hand,  if  the 
artery  can  be  felt  between  the  beats,  and  the  pulse  is  regular  and  of 
fair  size,  length  and  strength,  the  inference  is  that  the  amount  of 
leakage  into  the  auricle  is  slight. 

2.  The  degree  of  enlargement  of  the  left  side  of  the  heart. — 

The  position  of  the  apex  beat,  the  force  of  the  impulse  and  the 
outline  of  dulness  will  enable  the  observer  to  gauge  fairly  accurately 


MITRAL    INCOMPETENCE  179 

the  size  of  the  left  auricle  and  ventricle,  and  the  strength  of  the 
ventricular  contraction. 

Dilatation  of  the  auricle  and  ventricle  is,  to  a  certain  extent,  a 
conservative  process,  and  provided  it  is  not  excessive,  and  is  accom- 
panied by  adequate  hypertrophy,  as  shown  by  the  downward  dis- 
placement of  the  apex  beat  and  the  force  of  the  ventricular  con- 
traction, the  lesion  is  probably  slight. 

Great  enlargement  of  the  left  ventricle,  especially  in  an  outward 
direction,  is  indicative  of  serious  regurgitation. 

3.  The  degree  of  enlargement  of  the  right  ventricle. — A  moderate 
degree  of  hypertrophy  and  dilatation  of  the  right  ventricle  is  com- 
patible with  an  inextensive  mitral  lesion,  provided  dyspnoea  is  not 
easily  excited  and  there  is  an  absence  of  the  signs  of  pulmonic 
congestion. 

Great  increase  in  the  size  of  the  right  side  of  the  heart,  especially 
when  associated  with  shortness  of  breath  and  other  evidence  of 
pulmonic  engorgement,  is  indicative  of  serious  incompetence  of  the 
mitral  valve. 

4.  The  character  and  conduction  of  the  murmur  and  its  relation 
to  the  first  sound  of  the  heart. — Neither  the  intensity  nor  the  quality 
of  the  systolic  apical  bruit  affords  any  criterion  of  the  severity  of  the 
lesion,  though,  generally  speaking,  a  loud  or  long  murmur  denotes 
that  the  ventricle  is  acting  vigorously,  whereas  a  soft  or  short  one 
may  indicate  impending  failure  of  the  heart  Nor  can  the  manner 
in  which  the  murmur  is  conducted  be  said  to  have  much  significance 
with  respect  to  the  estimation  of  the  severity  of  the  lesion.  A  bruit 
audible  in  the  axilla  and  at  the  angle  of  the  left  scapula  may  accom- 
pany either  slight  or  extensive  regurgitation,  but,  as  a  rule,  the  greater 
the  amount  of  regurgitation,  the  better  is  the  murmur  propagated 
towards  the  left. 

It  is  to  the  effect  of  the  murmur  on  the  first  sound  of  the  heart 
that  attention  should  be  mainly  directed.  The  more  the  first  sound 
is  replaced  by  the  systoHc  bruit,  or,  in  other  words,  the  less  capable 
the  auriculo-ventricular  curtains  are  of  giving  rise  to  the  sound 
of  tension,  the  more  serious  is  the  incompetence  of  the  mitral 
valve. 

Thus  a  systolic  murmur  heard  at  the  apex,  'vih.ich.follows  and  does 
not  obscure  the  first  sound  and  is  not  audible  at  the  angle  of  the  left 
scapula,  denotes  that  the  leakage  through  the  mitral  opening  is 
slight. 

On  the  other  hand,  if  the  first  sound  is  totally  obscured  by  the 
murmur,  which  is  conducted  into  the  axilla  and  is  heard  at  the  angle 
of  the  left  scapula,  the  inference  is  that  the  amount  of  regurgitation 
is  very  considerable. 

5.  The  degree  of  accentuation  of  the  pulmonic  second  sound.— 

So  long  as  the  tricuspid  valve  is  competent,  the  amount  of  accentua- 
tion of  the  pulmonic  second  sound  forms  one  of  the  most  reliable 


iSo  DISEASES    OF    THE    HEART 

indications  of  the  degree  of  tension  in  the  blood  vessels  of  the  lungs, 
and  hence  of  the  extent  of  the  leakage  through  the  mitral  valve. 

6.  Tlie  severity  of  the  symptoms.— Provided  there  are  no 
comphcations  or  other  extraneous  exciting  cause,  and  there  is 
e%"idence  on  physical  examination  of  the  heart  of  well-developed 
compensatory  changes,  the  occurrence  of  severe  symptoms  is 
significant  of  serious  mitral  incompetence. 

To  recapitulate,  the  signs  of  an  inconsiderable  amount  of  re- 
gurgitation through  the  mirtral  valve  are :  (a)  a  pulse  of  fair  size, 
length  and  strength,  and  an  arterj'  that  can  be  felt  between  the 
beats  ;  (^)  moderate  enlargement  of  the  left  and  right  sides  of  the 
heart :  {c}  apical  systoHc  murmur  which  follows  and  does  not 
obscure  the  first  sound,  and  is  not  audible  at  the  angle  of  the  left 
scapula;  (d)  slight  accentuation  of  the  pulmonic  second  sound; 
and  (e)  the  absence  of  habitual  dyspncea,  cough,  etc.,  and  of  the 
signs  of  pulmonic  and  systemic  venous  congestion. 

On  the  other  hand,  the  signs  of  a  large  amount  of  leakage 
through  the  mitral  opening  are :  (a)  a  small,  weak,  short,  irregular 
pulse  of  low  tension ;  (b)  great  enlargement  of  both  sides  of  the 
heart  but  more  especially  of  the  right  ventricle ;  (c)  an  apical  systolic 
murmur  which  wholly  or  partially  obscures  the  first  sound ;  (d) 
well-marked  accentuation  of  the  pulmonic  second  sound ;  and  (<?) 
habitual  dyspnoea,  and  the  signs  of  pulmonic  and  systemic  venous 
congestion. 


CHAPTER  XII 
MITRAL  STENOSIS 


Pathogenesis — Morbid  anatomy — Patholc^ical  effects  on  the  Heart  and  C!cciikli«i 
— Symptoms — CompKcations — Physical  signs — ^Diagnosis — F.==timaHon  of  the 
degree  of  Stenosis. 

^ETIOLOGICAL  PATHOLOGY 

In  a  large  proportion  of  the  cases.,  obstnictive  disease  at  the  mitEal 
orifice  is  the  result  of  chronic  endocarditis  of  rheumatic  origin. 
Moreover,  this  variety  of  mitral  disease  appears  to  arise  much 
more  commonly  in  connection  with  the  slighter  manifestations  of 
rheumatism  than  with  the  more  acute  forms  of  the  disorcfer,  a 
fact  which  goes  far  to  explain  the  comparative  frequency  of  its 
occurrence  in  childhood  and  early  Hfe. 

Mitral  stenosis  has  also  been  ascribed  to  congenital  causes,  but 
the  weight  of  evidence,  both  pathological  and  cHniral,  is  largely 
against  this  mode  of  origin. 

In  a  considerable  number  of  instances,  narrowing  of  the  mhial 
orifice,  among  adults,  has  been  found  in  association  with  chronic 
renal  disease  and  arterio-sclerosis.  The  relation  between  the  valvular 
affection  and  the  renal  and  arterial  changes  has  not  yet  been  satis- 
factorily determined. 

Narrowing  of  the  mitral  aperture  has  been  attributed  to  an^mia^ 
by  reason  of  the  high  systemic  tension  and  consequent  initatioii 
to  which  the  mitral  valve  is  exposed  in  some  cases  of  this  disease. 

A  more  hkely  cause  of  irritation  of  the  valvular  segments  is  the 
more  or  less  constant  vibration  of  these  structures  that  is  maintained 
by  the  to-and-fro  flow  of  blood,  which  accompanies  the  mitral 
insufficiency  so  commonly  associated  with  anemia.  Moreover,  it 
is  to  be  expected  that  an  overgrowth  of  fibrous  tissue  in  the  valvular 
curtains  and  basal  ring  would  be  more  readily  excited  in  young 
ansemic  subjects  than  in  adults  by  irritation  of  this  kind- 

The  more  common  occurrence  of  mitral  stenosis  among  women 
than  men  may,  in  part  at  least  be  accounted  for  by  the  feet  that 
girls  suffer  from  chorea  and  aniemia  so  much  more  frequently  than 
boys. 

The   morbid   process  which  results  in   narrowing  of  die   mitral 

i8i 


i82  DISEASES   OF   THE    HEART 

orifice  usually  consists  in  a  gradual  and  progressive  fibrosis  of  the 
segments  of  the  valve,  chordae  tendineae,  and  basal  ring,  whereby 
these  structures  become  thickened,  rigid,  and  contracted. 

The  effect  of  these  changes  on  the  size  and  shape  of  the  opening 
varies  greatly  in  different  cases,  but  the  valvular  deformity  that  is 
produced  can  generally  be  included  under  one  of  two  kinds,  which 
have  been  termed  the  "funnel-shaped"  and  "button-hole"  varieties 
respectively. 

In  the  "  funnel-shaped  "  form  which  is  commonly  found  in  young 
subjects,  and  sometimes  in  old  people,  the  basal  ring  may  be  more 
or  less  contracted.  The  segments  of  the  valve  are  thickened,  and 
the  opening  they  inclose  is  constricted,  while  the  free  edges  of  the 
aperture  are  pulled  upon  by  shortened  and  rigid  chordse  tendinese, 
so  that  the  appearance  presented  by  the  valve  is  that  of  a  cone  with 
its  apex  pointing  into  the  ventricle. 

In  the  "  button-hole "  variety,  which,  with  few  exceptions,  is  the 
condition  found  in  adults,  the  basal  ring  is  greatly  thickened  and 
rigid.  The  curtains  of  the  valve  are  replaced  to  a  variable  extent 
by  dense  fibrous  tissue,  which  incloses  a  narrow  sHt  representing  the 
auriculo-ventricular  orifice.  The  chordae  tendine^e  and  muscuii 
papillares  may  participate  in  the  morbid  process,  and  are  often  found 
converted  into  a  thick  mass  of  fibrous  tissue. 

Calcic  and  other  salts  are  frequently  deposited  in  the  sclerosed 
tissue,  and  in  some  cases  the  mitral  orifice  is  transformed  into  a 
calcareous  ring. 

The  two  forms  of  valvular  deformity  may  be  variously  combined, 
with  corresponding  modifications  in  the  morbid  appearances. 

Obstruction  at  the  mitral  orifice  is  sometimes  caused  by  a  mass  of 
valvular  vegetations,  and  in  rare  instances  narrowing  of  the  opening 
has  been  produced  by  large  calcareous  nodules  in  the  muscular  wall 
of  the  ventricle  (Byrom  Bramwell). 

Stenosis  of  the  mitral  opening  is  usually  accompanied  by  some 
degree  of  incompetence  of  its  valve  on  account  of  the  inability  of 
the  thickened  rigid  and  distorted  curtains  to  adequately  close  the 
narrowed  orifice. 

PATHOLOGICAL  RESULTS 
Effect  on  the  Heart  and  Circulation 

The  earliest  effect  of  interference  with  the  passage  of  blood 
through  the  mitral  orifice  is  to  increase  the  work  of  the  left  auricle, 
and  thereby  to  produce  hypertrophy  of  its  walls.  Furthermore, 
since  the  lesion  in  the  large  majority  of  cases  is  progressive,  the 
additional  work  required  of  the  auricle,  and  therefore  the  amount  of 
its  hypertrophy,  increase  pari  passu  with  the  degree  of  obstruc- 
tion which  obtains. 

Sooner  or  later,  however,  owing  to  the  progressive  constriction  of 


MITRAL  STENOSIS  183 

the  mitral  orifice,  the  hypertrophied  auricle  becomes  unable  to  com- 
pletely discharge  its  contents  at  each  systole,  and  consequently  under- 
goes dilatation  from  incomplete  emptying,  that  is,  from  failure. 

The  interference  with  the  return  of  blood  from  the  lungs  that  is 
occasioned  by  the  gradual  increase  of  pressure  which  takes  place  in 
the  left  auricle  from  the  outset,  is  met  by  hypertrophy  of  the  right 
ventricle  and  a  general  rise  of  tension  in  the  pulmonic  circulation. 

The  occurrence  of  dilatation  of  the  left  auricle  aggravates  the 
difficulties  of  the  pulmonic  circulation,  and  in  this  way  gives  rise  to 
additional  hypertrophy  of  the  right  ventricle,  and  a  further  increase 
of  tension  in  the  blood  vessels  of  the  lungs. 

The  hypertrophy  of  the  right  ventricle  in  mitral  stenosis  is  greater 
than  in  any  other  form  of  valvular  disease  of  the  left  side  of  the 
heart.  Moreover,  the  congestion  of  the  pulmonic  circulation  and 
the  changes  produced  thereby  are  more  pronounced  than  in  mitral 
incompetence  on  account  of  the  greater  and  more  continuous  strain 
to  which  the  blood  vessels  of  the  lungs  are  exposed  in  mitral 
stenosis.  Thus  in  mitral  regurgitation  the  tension  in  the  left 
auricle  and  pulmonic  circulation  is  diminished  during  the  ven- 
tricular diastole,  whereas  in  mitral  stenosis  it  persists,  for  the  most 
part,  throughout  the  whole  cardiac  cycle. 

The  abnormally  high  blood  pressure  in  the  lungs  frequently  leads 
to  the  rupture  of  a  vessel,  hence  haemoptysis  is  not  an  uncommon 
symptom  in  cases  of  mitral  stenosis. 

Auscultatory  evidence  of  pulmonic  regurgitation  is  occasionally 
observed  in  association  with  mitral  stenosis.  Incompetence  of  the 
pulmonic  valve  under  these  circumstances  is  in  all  probability  due  to 
interference  with  the  valvular  mechanism  by  the  pressure  of  an 
enlarged  auricular  appendix,  in  which  blood  clotting  may  occur,  and 
is  not  due  to  chronic  forcing  of  the  valve,  else  it  would  be  found 
much  more  commonly  than  is  the  case. 

In  the  terminal  stages  of  mitral  obstruction,  dilatation  of  the 
left  auricle  is  usually  very  much  in  excess  of  hypertrophy,  and  in 
some  instances  the  enlargement  of  the  chamber  is  so  great  that 
pressure  is  exerted  on  surrounding  structures.  Moreover,  thrombosis 
is  apt  to  occur  in  the  dilated  left  auricle,  or  in  its  appendix,  on 
account  of  the  slowing  of  the  circulation  through  the  chamber.  The 
clots  thus  formed  are  sometimes  carried  into  the  blood  stream,  and 
by  this  means  give  rise  to  the  embolism  of  distant  organs. 

The  left  ventricle  in  mitral  stenosis  is  usually  found  either  un- 
altered or  slightly  diminished  in  size.  This  is  accounted  for  by 
the  fact  that  the  ventricle  receives,  on  the  whole,  a  smaller  quantity 
of  blood  than  usual  from  the  left  auricle,  and  has,  in  consequence, 
less  work  to  perform  in  the  propulsion  of  its  contents  into  the  aorta. 
In  the  advanced  stages  of  the  affection  the  diminished  supply  of 
blood  to  the  left  ventricle,  and  hence  to  the  aorta,  leads  to  a  con- 
siderable degree  of  arterial  ansemia.  Enlargement  of  the  left 
ventricle  {i.e.  hypertrophy  or  dilatation,  or  a  combination  of  the 


i84  DISEASES   OF   THE    HEART 

two  conditions),  which  is  observed  in  about  half  the  cases  of  mitral 
stenosis,  is  ascribable  to  an  initial  incompetence  of  the  valve,  or  to 
a  concurrent  local  cause,  such  as  pericarditis,  etc.,  or  to  an  extra- 
cardiac  affection,  as,  for  example,  chronic  renal  disease. 

The  adequacy  of  the  compensatory  changes  in  mitral  stenosis 
turns  on  the  extent  to  which  the  hypertrophied  left  auricle,  with 
the  help  of  the  hypertrophied  right  ventricle,  is  able  to  maintain  a 
sufficient  supply  of  blood  to  the  left  ventricle  and  aorta.  The  role 
of  the  left  auricle  in  this  respect  is  subsidiary  to  that  played  by  the 
right  ventricle,  which  bears  the  whole  brunt  of  the  pulmonic  circu- 
latory embarrassment. 

It  is  thus  easy  to  understand  the  important  influence  exerted  by 
pulmonary  complications  in  the  production  of  failure  of  the  right 
ventricle  in  mitral  stenosis. 

Compensation  may  be  maintained  for  years,  and  the  conditions  on 
which  its  duration  depend  have  already  been  considered  under  the 
head  of  mitral  regurgitation. 

The  breakdown  of  compensation  in  mitral  stenosis  may  be  due, 
in  the  first  instance,  to  dilatation  from  failure  either  of  the  left 
auricle  or  of  the  right  ventricle,  but  it  commonly  depends  on  the 
latter  cause. 

The  concurrent  establishment  of  tricuspid  incompetence  is  accom- 
panied by  a  fall  of  blood  pressure  in  the  lungs,  and  the  occur- 
rence of  general  venous  engorgement,  visceral  congestion  and  their 
effects  (see  pp.  172,  173). 

Dropsy  is  usually  a  late  phenomenon  in  mitral  stenosis,  and  is 
seldom  well  marked.  The  early  occurrence  of  oedema  may,  how- 
ever, be  observed  in  those  cases  in  which  obstruction  at  the  mitral 
orifice  is  combined  with  incompetence  of  the  valve. 

SYMPTOMS 

The  symptoms  of  mitral  stenosis  do  not  differ  materially  from 
those  observed  in  mitral  incompetence.  It  will  therefore  be 
unnecessary  to  do  more  than  emphasize  the  features  of  special 
interest  in  connection  with  the  symptoms  of  mitral  stenosis. 

It  occasionally  happens  that  the  discovery  of  the  physical  signs 
of  mitral  obstruction  precedes  the  occurrence  of  symptoms.  With 
a  slight  or  even  moderate  degree  of  stenosis  compensation  may  be 
maintained  for  years,  and  during  this  time  the  patient  suffers  little 
or  no  discomfort  of  any  kind. 

Shortness  of  breath  on  exertion,  accompanied  in  many  instances 
by  palpitation  and  a  feeling  of  tightness  or  constriction  of  the  chest, 
may,  for  considerable  periods,  be  the  only  indication  that  the  heart  is 
working  under  difficulty.     Pain  is  seldom  an  obtrusive  feature. 

Epistaxis  is  not  infrequently  observed  during  the  early  stages  of 
mitral  stenosis. 

Haemoptysis  is  often  an  early  symptom,  and  it  commonly  happens 


MITRAL   STENOSIS  185 

that  the  patient  seeks  advice  under  the  impression  that  he  is  suffering 
from  an  affection  of  the  lungs. 

Dyspepsia  or  an  attack  of  bronchitis  is  often  the  first  warning  of 
commencing  failure  of  compensation.  Symptoms  referable  to  con- 
gestion of  the  pulmonic  circulation  are  especially  obtrusive  during 
the  course  of  failing  compensation  in  cases  of  mitral  stenosis. 

Dyspnoea  is  always  a  prominent  feature  of  the  disease  under 
these  conditions,  and  paroxysmal  attacks  of  difficulty  in  breathing 
are  not  uncommon. 

Cough,  attended  by  the  expectoration  of  mucus,  which  is  often 
blood-stained,  may  be  a  troublesome  symptom. 

Attacks  of  bronchitis  are  of  frequent  occurrence,  and  are  a  fertile 
source  of  failure  of  the  right  ventricle. 

Patches  of  pneumonic  consolidation  or  of  pulmonary  apoplexy 
are,  also,  not  uncommonly  observed. 

The  influence  of  pulmonary  complications  in  the  production  of 
failure  of  the  right  ventricle  is  even  more  important  in  mitral 
stenosis  than  in  mitral  incompetence. 

A  type  of  mitral  stenosis,  which  has  been  insisted  on  by  Petit,  is 
characterised  by  the  presence  of  well-marked  aneemia  in  association 
with  dyspnoea,  palpitation,  constipation,  nervous  disturbances,  and 
catamenial  troubles. 

Emaciation  is  sometimes  a  very  prominent  feature  of  mitral 
stenosis,  more  especially  in  young  subjects. 

Embolic  manifestations  are  more  common  in  mitral  obstruction 
than  in  any  other  form  of  chronic  valvular  disease.  The  arteries 
of  the  brain,  spleen,  and  kidneys  are  the  vessels  most  frequently 
blocked.  The  plugging  of  a  cerebral  artery  may  be  followed  by 
necrosis  of  the  area  of  brain  supplied  by  the  vessel.  On  the  other 
hand,  the  function  of  the  affected  part  is  frequently  wholly  or 
partially  restored  by  the  establishment  of  a  collateral  circulation. 
Dilatation  of  the  right  ventricle  from  failure,  as  in  mitral  regurgitation, 
leads  to  the  signs  and  symptoms  of  portal  and  systemic  venous 
stagnation.  Dropsy,  however,  is  rarely  well  marked  in  mitral 
stenosis,  and  as  a  rule  does  not  appear  until  the  terminal  stages 
of  the  disease.  The  reason  for  this  is  not  fully  understood.  Should 
dropsy  occur  at  an  early  stage  of  the  disorder,  the  stenosis  is  almost 
invariably  found  to  be  associated  with  incompetence  of  the  mitral 
valve.  Extreme  dropsy  in  mitral  stenosis  is,  as  Sir  William  Broad- 
bent  has  pointed  out,  highly  suggestive  of  concomitant  tricuspid 
obstruction. 

PHYSICAL  SIGNS 

Physiognomy. — The  crimson  lips  and  bright  pink  flush  on  either 
cheek,  which  are  so  often  observed  in  cases  of  stenosis  of  the  mitral 
orifice,  form  a  striking  contrast  to  the  appearance  presented  by  the 
subjects  of  incompetence  of  this  valve. 


i86  DISEASES   OF   THE    HEART 

The  complexion  in  mitral  stenosis  has  not,  however,  always  these 
characters.  In  some  instances  the  face  exhibits  the  signs  of 
ansemia,  and  is  of  a  pale,  sallow  colour ;  while  in  others,  and 
especially  when  the  stenosis  is  associated  with  well-marked  incom- 
petence of  the  mitral  valve,  the  lips  and  cheeks  present  a  dusky 
hue,  suggestive  of  imperfect  aeration  of  the  blood.  In  the  terminal 
stages  of  the  disorder,  when  failure  of  the  right  ventricle  has  super- 
vened, the  appearance  of  the  patient  resembles  that  seen  in  cases  of 
mitral  incompetence. 

Pulse.— So  long  as  compensation  is  maintained  the  pulse  is 
regular,  both  in  force  and  frequency.  The  artery  is  small,  and  can 
be  felt  between  the  beats,  but  is  easily  compressible.  The  pulse 
wave  is  small,  long,  and  easily  obliterated  by  pressure  with  the 
finger. 

When  compensation  fails,  and  the  tricuspid  valve  becomes  in- 
competent, the  pulse  becomes  extremely  irregular,  both  in  force 
and  frequency.  If  stenosis  of  the  mitral  orifice  is  associated  with 
incompetence  of  its  valve,  the  pulse  is  usually  irregular  from  the 
beginning. 

The  condition  of  virtual  tension  of  the  pulse,  which  is  present 
in  cases  of  mitral  stenosis  until  a  late  period  of  the  disease,  is  of 
considerable  interest,  and  is  probably  the  outcome  of  reflex  vaso- 
motor influences,  whereby  the  systematic  vessels  contract  down  on 
their  diminished  contents.  In  the  presence  of  chronic  renal  disease 
this  explanation  is,  of  course,  unnecessary. 


HEART 

Inspection. — Bulging  of  the  prsecordial  region  is  very  rareljr 
observed  in  uncomplicated  cases  of  mitral  stenosis.  The  apex 
beat  is  seen  in  its  normal  position,  or  it  may  be  displaced  slightly 
outwards  and  downwards. 

A^isible  pulsation  is  occasionally  manifested  in  young,  thin  sub- 
jects, in  the  second  and  third  left  intercostal  spaces  close  to  the 
sternum,  and  is  supposed  to  be  due  to  the  systole  of  the  enlarged 
left  auricle. 

The  forcible  contraction  of  the  hypertrophied  right  ventricle 
frequently  gives  rise  to  epigastric  pulsation. 

Palpation. — The  apex  beat  is  usually  ill  defined,  but  the  im- 
pulse of  the  left  ventricle  is,  as  a  rule,  fairly  distinct,  and  communi- 
cates to  the  hand  the  sensation  of  a  short,  sharp  shock,  or  tap. 

Palpation  in  the  region  of  the  apex  beat  frequently  reveals  the 
presence  of  a  peculiar  vibratory  thrill,  which  immediately  precedes, 
and  terminates  abruptly  in  the  ventricular  impulse.  Pulsation  over 
the  right  ventricle  is  diffused,  forcible,  and  heaving.     The  ventricular 


MITRAL   STENOSIS  187 

impulse  is  felt  most  distinctly  when  the  hand  is  placed  over  the 
epigastrium. 

Percussion. — The  area  of  cardiac  dulness  is  increased  upwards, 
and  to  the  right,  and  in  some  instances  to  the  left  also.  The  upper 
limit  of  dulness  may  reach  to  the  level  of  the  third  or  even  second 
rib,  and  is  due  to  dilatation  and  hypertrophy  of  the  left  auricle. 

When  the  enlargement  of  the  right  ventricle  is  well  marked,  the 
line  of  dulness  may  extend  laterally  beyond  the  right  sternal  edge. 

In  uncomplicated  cases  of  mitral  stenosis  the  left  ventricle  is  not 
enlarged ;  in  point  of  fact,  it  is  often  somewhat  smaller  than  usual. 
Consequently  there  is  little  or  no  alteration  in  the  left  limit  of 
cardiac  dulness,  or  in  the  position  of  the  apex  of  the  heart.  An 
increase  of  the  cardiac  dulness  to  the  left,  with  displacement  of  the 
apex  beat  outwards  and  downwards,  depends  mainly  on  dilatation 
and  hypertrophy  of  the  left  ventricle,  which  is  most  commonly  due 
to  concurrent  incompetence  of  the  mitral  valve.  It  may  also  depend 
on  other  causes,  as,  for  example,  peri-  or  myocarditis,  chronic  renal 
disease,  etc. 

Auscultation. — At  the  apex  a  rough  vibratory  presystolic  murmur 
is  heard,  which  runs  up  to,  and  terminates  abruptly  in  a  short,  sharp 
and  loud  first  sound.  The  first  sound,  in  this  situation,  may  also 
be  accompanied  or  followed  by  a  soft  blowing  systolic  bruit,  indica- 
tive of  concurrent  mitral  incompetence.  The  second  sound  may 
or  may  not  be  audible  at  the  apex.  The  presence  or  absence  of 
the  second  sound  at  and  to  the  left  of  this  point  is  determined  by 
the  degree  of  mitral  narrowing  which  obtains. 

At  the  base  the  second  sound  is  frequently  reduplicated,  and  a 
similar  phenomenon  is  sometimes  observed  at  the  apex. 

In  certain  instances  the  double  sound  is  audible  at  the  apex  only^ 
and  the  sign  is  then  of  considerable  diagnostic  significance,  in  so 
far  as  it  is  one  of  the  earliest  indications  of  commencing  obstruction 
at  the  mitral  orifice  (see  p.  53). 

Over  the  pulmonic  cartilage  the  second  sound  is  accentuated, 
while  in  the  aortic  area  it  is  either  unaltered  or  somewhat  dimin- 
ished in  intensity. 

Several  of  the  foregoing  physical  signs  require  more  detailed 
consideration. 

In  typical  cases  the  presystolic  murmur  is  peculiarly  rough  and 
rumbling  in  character,  and  it  increases  in  intensity  up  to  its  abrupt 
termination  in  the  first  sound. 

As  a  rule  the  murmur  is  audible  over  a  very  limited  area,  which 
is  situated  just  above  and  internal  to  the  apex  beat.  It  is  very 
rarely  propagated  into  the  left  axilla,  nor  can  it  be  heard  at  the 
angle  of  the  left  scapula.  In  exceptional  instances,  however,  a  very 
loud  bruit  is  audible  in  both  these  situations.  It  occasionally 
happens,  too,  that  the  murmur  is  conducted  towards  the  right,  when 


i88  DISEASES   OF   THE    HEART 

it  may  be  heard  along  the  left  sternal  edge  as  high  as  the  third  rib 
or  second  interspace. 

The  characteristic  features  of  the  presystolic  bruit,  therefore,  are 
its  peculiar  quality,  singular  intensity,  and  the  limited  area  of  its 
audibility. 

It  is,  however,  not  the  only  kind  of  diastolic  murmur  associated 
with  mitral  stenosis. 

During  the  period  distinguished  by  Sir  William  Broadbent  as 
the  second  stage  of  the  disorder,  the  diastolic  murmur  is  extremely 
variable  and  inconstant.  The  different  modifications  of  the  dia- 
stolic murmur  which  may  be  observed  are  conveniently  classified 
as  follows : — 

1.  The  early  diastolic  murmur  (or,  as  it  is  sometimes   termed, 

the  post-systolic  murmur). 

2.  The  mid-diastolic  murmur. 

3.  The  late  diastolic,  presystolic,  or  auriculo-systolic  murmur, 

4.  The  entire  diastolic  murmur. 

The  different  varieties  of  the  diastolic  murmur  may  be  repre- 
sented diagrammatically  (see  opposite  page). 

The  early  diastolic  bruit  is  of  somewhat  rare  occurrence  as  an 
isolated  murmur  in  mitral  stenosis,  but  when  present  it  closely 
follows  the  second  sound,  and  is  audible  during  the  beginning  only 
of  the  diastolic  period.  It  is  a  short  bruit,  of  variable  character, 
and  exceedingly  inconstant,  so  that  it  may  even  appear  and  dis- 
appear during  the  time  of  examination. 

A  murmur  occupying  the  middle  portion  of  the  diastole  has 
been  termed  mid-diastohc.  It  resembles  the  foregoing  bruit  both 
in  character  and  in  the  irregularity  of  its  appearance. 

The  presystolic  variety  of  the  diastolic  murmur  has  already  been 
described  and  is  the  one  most  frequently  heard  in  cases  of  mitral 
stenosis. 

A  bruit  occupying  the  whole  of  the  diastolic  period  is  of  fairly 
common  occurrence  in  mitral  stenosis,  and  is  termed  the  entire 
diastolic  murmur.  It  commences  immediately  after  the  second 
sound,  and  during  the  latter  part  of  the  diastole  it  gradually  in- 
creases in  roughness  and  intensity  up  to  its  abrupt  termination  \u 
the  first  sound. 

The  murmur  may  be  cut  into  two  portions  by  an  appreciabk 
interval,  so  that  the  sequence  of  events  is  a  diastolic  bruit  im- 
mediately following  the  second  sound  (early  diastolic  murmur), 
then  a  period  of  quiet,  succeeded  by  a  late  diastolic  or  presystolic 
murmur,  running  up  to  the  first  sound. 

The  method  of  production  of  the  different  varieties  of  the 
diastolic  murmur,  and  the  conditions  under  which  each  one  is 
occasioned,  will  now  be  briefly  considered. 


MITRAL     STENOSIS 


189 


Diastolic  Murmurs 


FIG.  38.       DIAGRAMMATIC    REPRESENTATION 
OP   AN    ENTIRE   DIASTOLIC    MURMUR 


FIG.   39.       DIAGRAMMATIC    REPRESENTATION 
OF  A   PRESYSTOLIC   MURMUR 


FIG.  40.       DIAGRAMMATIC   REPRESENTATION  FIG.  4I.       DIAGRAMMATIC    REPRESENTATION 

OF   AN    EARLY   DIASTOLIC    MURMUR  OF   A    MID-DIASTOLIC    MURMUR 


I90  DISEASES    OF   THE    HEART 

In  compensated  cases  of  mitral  obstruction  the  forces  concerned 
in  the  propulsion  of  blood  through  the  narrowed  auriculo-ventricular 
orifice  into  the  left  ventricle  are : — 

1.  The  high   pressure  in  the  pulmonic  vessels  and   left   auricle 

which  is  maintained  by  the  hypertrophy  of  the  right  ventricle. 

2.  The  force  of  the  auricular  systole. 

3.  The  suction  power  of  the  left  ventricle  during  diastole. 

Provided  these  forces,  either  separately  or  collectively,  are  suffi- 
ciently powerful,  during  any  period  of  the  diastole  of  the  heart,  to 
bring  about  the  requisite  swiftness  of  flow  through  the  narrowed 
mitral  opening  into  the  left  ventricle,  a  "  fluid  vein  "  is  formed- 
Consequently  the  conditions  necessary  for  the  production  of  a 
murmur  are  present. 

The  variety  of  diastolic  bruit  which  is  produced  depends  on 
the  period,  during  the  diastole,  at  which  the  above  conditions  are 
fulfilled. 

Thus  they  may  be  present  during  the  auricular  systole  only,  or 
during  the  active  dilatation  of  the  left  ventricle,  or  they  may  obtain 
during  the  whole  diastole  with  the  production  of  presystolic,  early 
diastolic,  and  entire  diastolic  murmurs  respectively. 

The  loudness  of  the  murmur  depends  mainly  on  the  rapidity  of 
the  blood  current.  It  is  on  this  account  that  the  presystolic  bruit  is 
usually  so  intense,  for  the  forces  urging  the  blood  into  the  ventricle 
are  all  combined  during  the  time  of  the  auricular  systole,  and  this 
is  the  period  during  which  the  murmur  in  question  is  produced. 

It  is  beyond  the  scope  of  this  work  to  consider  the  objections 
which  have  been  raised  against  these  views,  and  it  must  suffice  that 
the  explanations  given  above  are  those  accepted  by  the  majority 
of  observers. 

The  cause  of  the  short,  sharp  first  sound  in  mitral  stenosis  has 
been  the  subject  of  considerable  discussion,  and  is  still  a  matter 
of  dispute. 

It  has  been  ascribed  to  the  sudden  and  forcible  contact  of  the 
mitral  curtains,  which,  in  consequence  of  the  imperfect  distension 
of  the  left  ventricle,  are  not  so  gradually  floated  up  or  so  perfectly 
adapted  to  each  other  during  diastole  as  obtains  under  normal 
conditions. 

Dr.  Sansom  considers  that  such  forcible  contact  of  the  mitral 
segments  during  the  ventricular  systole  is  impossible,  both  on  phy- 
siological and  mechanical  grounds.  He  suggests  that  the  sound 
is  produced  on  the  right  side  of  the  heart,  and  is  due  to  the  rapid 
and  vigorous  action  of  the  right  ventricle  acting  in  the  face  of 
considerable  resistance,  whereby  the  wall  of  this  chamber,  in  con- 
junction with  the  tricuspid  valvular  curtains,  gives  rise  to  the 
"sudden  sound  of  tension." 

An  objection  to  this  view  is  the  fact  that  the  occurrence  of  failure 


MITRAL   STENOSIS  191 

of  the  right  ventricle  is  not  followed  by  any  alteration  in  the  character 
of  the  first  sound. 

Sir  William  Broadbent  has  proposed  another  explanation.  He 
supposes  that  in  consequence  of  the  imperfect  filling  of  the  left 
ventricle  the  wall  of  this  chamber  is  suddenly  "  brought  up "  taut 
on  its  contents  after  a  portion  of  the  systole  is  completed. 

The  disappearance  of  the  second  sound  at  and  to  the  left  of  the 
apex,  which  is  observed  when  the  constriction  of  the  mitral  opening 
is  at  all  considerable,  has  been  ascribed  by  Broadbent  to  (i)  the 
weakening  of  the  aortic  second  sound,  consequent  on  the  lessened 
diastolic  tension  of  the  aortic  semilunar  valves  that  follows  a 
diminished  supply  of  blood  to  the  aorta,  and  (2)  the  displacement 
from  the  chest  wall  of  the  left  ventricle,  which  normally  conducts 
the  aortic  second  sound  to  the  apex,  by  the  enlarged  right  heart. 

The  last  stage  of  mitral  stenosis  is  characterized  by  the  absence 
of  the  presystolic  murmur,  so  that  all  that  is  heard  at  the  apex  is 
a  short,  sharp  first  sound  with  or  without  a  systolic  bruit.  

The  disappearance  of  the  presystolic  murmur  is  due  to  the 
development  of  tricuspid  incompetence  which  leads  to  a  fall  of 
pressure  in  the  pulmonic  circulation.  The  effect  of  this  is  that  the 
auricular  systole  now  drives  blood  backwards  as  well  as  forwards, 
and  the  flow  into  the  left  ventricle  is  not  sufficiently  forcible  to 
generate  a  murmur.  At  the  same  time,  the  accentuation  of  the 
pulmonic  second  sound  is  lost,  and  a  systolic  bruit,  due  to  tricuspid 
regurgitation,  may  become  audible  over  the  ensiform  cartilage. 

The  concomitant  signs  of  insufficiency  of  the  tricuspid  valve  are 
distension  of  the  jugular  veins,  enlargement  of  the  liver,  and  con- 
gestion of  the  systemic  and  portal  venous  circulations,  together  with 
its  effects. 

In  the  terminal  stages  of  mitral  stenosis  the  liver  may  fail  to 
enlarge  on  account  of  the  supervention  of  cirrhosis  of  the  organ, 
induced  by  long-continued  venous  congestion.  This  event  makes 
the  prognosis  more  serious,  and  may  be  a  cause  of  persistent  ascites, 
even  vi^hen  there  is  little  or  no  general  oedema. 

Dropsy  usually  appears  late  in  mitral  stenosis,  and  is  seldom  well 
marked. 

The  early  occurrence  of  dropsy  in  mitral  obstruction  will  generally 
be  found  to  depend  on  concurrent  incompetence  of  the  mitral  valve. 

If  the  dropsy  is  extreme,  stenosis  of  the  tricuspid  orifice  is  probably 
also  present. 

DIAGNOSIS 

If  aortic  regurgitation  can  be  excluded,  an  apical  presystoHc 
murmur  presenting  the  characters  previously  described  is  pathog- 
nomonic of  mitral  stenosis. 

In  those  instances,  however,  in  which  the  signs  of  aortic  in^ 
competence  are  observed  in  association  with  an  apical  presystolic 


192  DISEASES   OF   THE   HEART 

thrill  and  murmur,  or  murmur  only,  the  diagnosis  of  mitral  narrow- 
ing should  be  made  with  very  great  caution. 

The  two  lesions  sometimes  coexist,  but  since  the  auscultatory 
phenomena  of  mitral  stenosis,  so  far  as  the  presystolic  murmur  is 
concerned,  may  be  exactly  simulated  (see  p.  203)  by  those  of  aortic 
incompetence,  it  is,  under  the  circumstances  mentioned  above,  often 
extremely  difficult  and  occasionally  impossible  to  decide  positively 
whether  the  latter  affection  is  or  is  not  comphcated  by  the  former. 

The  differential  diagnosis  must  be  based  on  a  general  considera- 
tion of  the  whole  of  the  symptoms  and  physical  signs,  assisted  by 
the  cardiographic  and  sphygmographic  evidence. 

If  the  presystolic  murmur  is  wanting,  as  is  the  case  in  the  final 
stage  of  the  disease,  the  short,  sharp  first  sound  of  mitral  stenosis 
may  be  mistaken  for  that  of  dilatation  of  the  heart.  The  absence 
of  the  second  sound  at  and  to  the  left  of  the  apex  would,  however 
establish  the  diagnosis  of  mitral  stenosis. 

A  rumbling  presystolic  murmur  is  sometimes  heard  in  the  mitral 
area  after  an  attack  of  pericarditis  or  in  association  with  pericardial 
adhesions  in  the  case  of  children.  The  murmur  heard  under  these 
circumstances  has  not  the  peculiar  vibratory  character  of  the  bruit 
audible  in  cases  of  mitral  narrowing,  nor  does  it  terminate  abruptly 
in  the  first  sound.  Furthermore,  the  first  sound  does  not  present 
the  characteristic  modification  observed  in  mitral  stenosis. 

The  association  of  regurgitation  through  the  mitral  opening  with 
narrowirig  of  the  orifice  sometimes  leads  to  difficulty  in  the  detection 
of  the  latter  affection  in  the  absence  of  the  presystolic  murmur. 

The  diagnosis,  in  this  event,  turns  largely  on  the  characters  of  the 
first  sound  at  the  apex,  since  the  effect  of  regurgitation  is  to  obscure 
and  destroy  it,  whereas  the  effect  of  stenosis  is  to  shorten  and  ex- 
aggerate it.  If  therefore  the  first  sound  at  the  apex  is  short  and  loud, 
and  is  followed  and  not  obscured  by  a  systolic  bruit,  which  is  neither 
well  conducted  into  the  left  axilla,  nor  audible  at  the  angle  of  the 
left  scapula,  the  presence  of  mitral  stenosis  may  reasonably  be  sus- 
pected. The  absence  of  the  second  sound  at  and  to  the  left  of 
the  apex  would  be  further  evidence  in  favour  of  the  existence  of 
mitral  narrowing. 

Moreover,  if  the  symptoms  and  physical  signs  of  pulmonary  con- 
gestion and  enlargement  of  the  right  ventricle,  associated  with  an 
apical  systolic  murmur,  are  more  marked  than  the  amount  of 
regurgitation  through  the  mitral  orifice,  estimated  on  other  grounds, 
would  account  for,  the  possibility  of  such  a  complication  as  mitral 
stenosis  must  be  taken  into  consideration. 

It  appears  also  that  regurgitation  through  the  mitral  orifice  would 
occur  much  more  commonly  in  association  with  mitral  stenosis 
were  it  not  that  the  high  pressure  in  the  left  auricle  during  the 
ventricular  systole  is  sufficient  to  prevent  any  reflux  through  the 
imperfectly  closed  auriculo-ventricular  aperture  (Samways). 


MITRAL   STENOSIS  193 


ESTIMATION    OF    THE    DEGREE    OF    NARROWING    IN 
MITRAL    STENOSIS 

The  extent  of  the  lesion  is  determined  by  a  consideration  of  the 
following  data : — 

I.  Tlie  pulse. — So  long  as  the  pulse  is  regular  in  force  and 
frequency  and  the  artery  is  of  medium  size,  the  amount  of  mitral 
narrowing  cannot  be  very  great. 

Great  reduction  in  the  size  of  the  artery  and  a  small,  weak,  and 
extremely  irregular  pulse  are  among  the  indications  of  severe 
obstruction. 

2.  The  degree  of  enlargement  of  the  left  auricle. — The  increase 
of  dulness  in  the  third  and  fourth  intercostal  spaces,  immediately 
to  the  left  of  the  sternum,  will  indicate  roughly  the  size  of  the  left 
auricle. 

3.  The  degree  of  enlargement  of  the  right  ventricle. — The  size 
of  this  chamber  and  the  force  of  the  ventricular  contraction  furnish 
the  most  reliable  evidence  of  the  extent  of  the  mitral  narrowing, 
since  it  is  on  this  side  of  the  heart  and  on  the  left  auricle  that  the 
stress  of  the  lesion  falls. 

4.  The  presence  or  absence  of  the  aortic  second  sound  at  and  to 
the  left  of  the  apex. — If  the  second  sound  is  audible  at  and  to  the 
left  of  the  apex  the  degree  of  stenosis  is  probaby  slight,  for  the 
reasons  which  have  already  been  given. 

The  absence  of  the  second  sound  in  this  situation  is  an  indication 
that  the  narrowing  of  the  orifice  is  considerable. 

5.  The  amount  of  accentuation  of  the  pulmonic  second  sound. — 

In  the  absence  of  pulmonary  complications  and  provided  the 
tricuspid  valve  is  competent,  the  degree  of  pronunciation  of  the 
pulmonic  second  sound  affords  a  means  of  gauging  the  blood 
pressure  in  the  lungs,  and  hence  of  estimating  the  degree  of 
obstruction  to  which  the  lesion  has  given  rise. 

6.  The  severity  of  the  arterial  anaemia  and  venous  engorge- 
ment.^ So  long  as  there  are  no  complications,  and  provided  the 
compensatory  changes  are  well  developed,  the  presence  of  marked 
arterial  anaemia  and  venous  engorgement  is  significant  of  serious 
obstruction. 

In  order  to  facihtate  the  estimation  of  the  extent  of  the  lesion, 
and  to  serve  as  a  guide  to  the  prognosis  in  mitral  stenosis,  Sir  W. 
o 


194  DISEASES    OF   THE    HEART 

Broadbent  has  divided  the  progress  of  the  disease  into  three  stages, 
which  are  as  follows  : — ■ 

1.  The  first  stage  which  is  characterised  by — 

(a)  A  presystolic  murmur 

(3)  The  gradual  development  of  a  short  and  sharp  first  sound 

at  the  apex 
(c)  Accentuation  and  reduplication  of  the  pulmonic  second 

sound. 

2.  The  second  stage  which  is  characterized  by — 

(a)  The  disappearance  of  the  second  sound  at  and  to  the  left 

of  the  apex 

(b)  A  short,  sharp  first  sound 

(c)  A  variable  diastolic  murmur 

3.  The  third  stage  which  is  characterized  by — 

(a)  The  disappearance  of  the  presystolic  murmur 
(l?)  A  short  and  sharp  first  sound 
(c)  A  tricuspid  systolic  murmur 

In  the  light  of  what  has  already  been  said  with  regard  to  the 
estimation  of  the  degree  of  obstruction  at  the  mitral  opening,  a 
further  explanation  of  these  stages  is  unnecessary. 

It  may,  however,  be  pointed  out  that  under  this  classification, 
which  is  based  on  auscultatory  signs,  the  second  and  third  stages 
are  interchangeable.  Thus  a  case  which  has  reached  the  third  stage 
may,  under  favourable  conditions  and  by  means  of  suitable  treat- 
ment, be  restored  to  the  second,  a  feature  that  does  not  obtain 
with  respect  to  the  first  two  stages. 


CHAPTER    XIII 
AORTIC    INCOMPETENCE 


Pathogenesis — Morbid  Anatomy — Effects  on  the  Heart  and  Circulation  — 
Compensation — Sudden  Death — Symptoms — CompHcations — Physical  Signs 
— Diagnosis — Estimation  of  the  Amount  of  Regurgitation. 

^ETIOLOGICAL    PATHOLOGY 

The  chief  causes  of  aortic  incompetence  are:  (i)  Acute,  sub-acute, 
or  chronic  valvuHtis  of  rheumatic,  and  probably,  in  some  instances, 
of  syphiUtic  origin;  (2)  chronic  valvulitis  (sclerosis)  due  to  pro- 
longed muscular  strain;  and  (3)  atheroma,  which  may  attack  the 
valve  primarily,  or  as  the  result  of  the  extension  of  the  morbid 
process  from  the  root  of  the  aorta. 

Syphilis  and  chronic  alcoholism  frequently  co-operate  with 
mechanical  strain  in  the  production  of  aortic  valvular  disease ;  they 
are  also  important  factors  in  the  causation  of  atheroma. 

It  is  often  impossible  to  distinguish  between  the  effects  of  strain 
and  atheroma,  since  they  are  both  the  result,  for  the  most  part,  of  a 
common  cause,  viz.  increased  arterial  tension. 

As  the  result  of  the  operation  of  one  or  other  of  the  morbid  pro- 
cesses above  mentioned,  the  free  margins  of  the  aortic  cusps  become 
thickened,  rigid,  and  retracted,  or  otherwise  deformed,  so  that  their 
proper  adaptation  is  rendered  impossible. 

The  sclerosed  tissue  is  often  the  seat  of  ulcerative  changes,  which 
may  lead  to  perforation,  laceration,  or  rupture  of  a  flap,  and  thus 
to  incompetence  of  the  valve.  It  is  also  not  uncommon  to  find 
the  thickened  segments  infiltrated  with  calcareous  salts. 

In  some  instances  the  proper  adaptation  of  the  cusps  of  the  valve 
is  prevented  by  a  growth  of  vegetations. 

Rupture  of  a  segment  of  a  healthy  aortic  valve  is  occasionally  due 
to  sudden  and  violent  strain.  External  violence — to  wit,  a  blow  on 
the  outside  of  the  chest — has  in  a  few  cases  been  the  cause  of  the 
rupture  af  an  aortic  cusp. 

In  rare  instances  aortic  incompetence  occurs  as  a  congenital 
lesion. 

19s 


196  DISEASES   OF  THE    HEART 

Dilatation  of  the  root  of  the  aorta  may  involve  the  orifice  of  the 
vessel,  and  by  this  means  may  give  rise  to  relative  incompetence  of 
the  valve.     The  lesion  is,  however,  of  rare  occurrence. 

The  valvular  changes  which  lead  to  aortic  incompetence  are  fre- 
quently, indeed  usually,  accompanied  by  some  induration  of  the 
fibrous  ring  surrounding  the  orifice  of  the  vessel.  The  subsequent 
contraction  of  the  cicatricial  tissue  leads  to  more  or  less  constric- 
tion of  the  opening,  with  the  result  that  valvular  incompetence  is 
commonly  combined  with  a  variable  degree  of  narrowing  of  the 
aortic  aperture. 


PATHOLOGICAL   RESULTS 
Effects  on  the  Heart  and  Circulation 

In  consequence  of  the  valvular  incompetence,  a  certain  quantity 
of  blood  flows  backwards  from  the  aorta  into  the  left  ventricle 
during  its  diastole.  The  ventricle  is,  therefore,  now  supplied  from 
two  sources,  and  at  the  end  of  diastole  its  contents  exceed  the 
normal  by  the  amount  which  has  returned  from  the  aorta.  The 
accommodation  of  this  additional  quantity  of  blood  necessitates 
an  increase  in  the  capacity  of  the  chamber,  which  can  be  effected 
only  by  the  stretching  of  its  elastic  walls.  This  process,  if  con- 
tinued, becomes  dilatation;  hence  the  earliest  effect  of  aortic 
incompetence  is  to  produce  dilatation  of  the  left  ventricle  from 
overfilling.  The  increased  work  involved  in  the  propulsion  of  a 
larger  amount  of  blood  than  normal  leads  to  hypertrophy  of  the 
ventricular  walls,  provided,  of  course,  the  myocardium  enjoys 
sufficient  nutrition. 

There  is,  however,  a  further  and  more  important  cause  of  dilata- 
tion and  hypertrophy  of  the  left  ventricle  in  aortic  insufficiency, 
inasmuch  as  the  ventricle  has  to  withstand,  during  its  diastole,  the 
distending  effects  of  the  regurgitant  stream  under  the  pressure  of 
the  arterial  recoil. 

The  strain  imposed  on  the  walls  of  the  ventricle  by  this  means 
will  vary  with  the  extent  of  the  lesion  and  the  state  of  arterial 
tension.  It  is  probably  considerable  in  all  cases,  and  constitutes 
the  chief  source  of  overwork  which  has  to  be  performed  by  the 
ventricle. 

Dilatation  would  quickly  get  the  upper  hand  of  hypertrophy  at 
the  outset  were  it  not  that  the  ventricle  falls  back  on  its  reserve 
power,  which  temporarily  staves  off  the  distending  effects  of  the 
lesion.  The  subsequent  occurrence  of  hypertrophy  restores  and 
maintains  the  tone  of  the  ventricle,  and  prevents  more  dilatation  of 
the  chamber  than  is  necessary  to  accommodate  the  amount  of  blood 
by  which  it  is  overcharged. 

If  hypertrophy  did  not  occur,   the  reserve  power  of  the  heart 


AORTIC   INCOMPETENCE  197 

would  soon  become  exhausted,  and  there  is  then  no  reason  why 
dilatation  of  the  ventricle  should  not  proceed  indefinitely. 

The  relative  proportions  of  hypertrophy  and  dilatation  of  the  left 
ventricle  determine  in  a  great  measure  the  adequacy  of  compensation 
in  aortic  incompetence. 

The  high  tension  which  prevails  in  the  left  ventricle  during  its 
diastole  interferes  with  the  flow  of  blood  through  the  mitral  orifice, 
and  thus  leads  to  a  rise  of  pressure  in  the  left  auricle,  pulmonic 
circulation,  and  right  ventricle.  The  intensity  of  this  process 
depends  largely  on  the  rate  of  development  and  extent  of  the  lesion, 
and  on  the  degree  of  adequacy  of  the  compensatory  changes. 

If  the  valvular  incompetence  comes  on  slowly,  and  is  of  moderate 
severity,  and  provided  also  that  compensation  is  satisfactory,  there 
is  apparently  little  or  no  serious  interference  with  the  pulmonic 
circulation.  In  some  instances,  however,  owing  either  to  the  sudden 
development  or  to  the  severity  of  the  lesion,  or  to  the  relative 
or  absolute  inadequacy  of  the  compensatory  changes,  or,  as  most 
commonly  happens,  to  a  combination  of  these  conditions,  more 
or  less  embarrassment  of  the  pulmonic  circulation  is  produced. 
The  left  auricle  consequently  undergoes  dilatation  and  occasion- 
ally some  hypertrophy,  while  the  right  ventricle  usually  becomes 
hypertrophied. 

In  the  late  stages  of  aortic  insufficiency,  the  left  ventricle  under- 
goes dilatation  from  failure,  a  process  that  is  attended  by  relative 
incompetence  of  the  mitral  valve  whereby  the  circulation  through 
the  lungs  is  still  further  hampered. 

In  many  cases,  too,  the  aortic  lesion  is  associated  with  organic 
changes  in  the  mitral  valve  which  may  render  it  incompetent. 

Dilatation  of  the  right  ventricle  from  failure  ultimately  super- 
venes, and  the  consequent  establishment  of  tricuspid  regugitation 
is  followed  by  the  usual  sequence  of  events,  culminating  in  general 
venous  stasis,  visceral  congestion,  and  dropsy. 

The  most  striking  and  characteristic  features  of  acrtic  incompe- 
tence are,  however,  observed  in  connection  with  its  effects  on  the 
arterial  circulation. 

In  the  first  instance  the  supply  of  blood  to  the  aorta  and  peripheral 
vessels  is  diminished  by  the  amount  which  regurgitates  into  the  left 
ventricle  during  each  diastole,  so  that  a  variable  degree  of  arterial 
anaemia  is  produced.  Provided,  however,  the  dilatation  and  hyper- 
trophy of  the  left  ventricle  are  adequate,  the  quantity  of  blood 
thrown  into  the  aorta  at  each  systole  exceeds  the  normal  by  the 
amount  which  flows  backwards  during  diastole,  and  in  this  way 
the  ordinary  balance  of  the  circulation  is  restored.  The  excessive 
strain  to  which  the  arterial  system  is  subjected  in  consequence 
of  the  more  forcible  injection  of  a  larger  quantity  of  blood  than 
usual  into  the  aorta,  has  important  effects  on  the  walls  of  these 
vessels,  in  that  they  become  stretched  and  thickened,  and  frequently 
show  atheromatous  changes. 


198  DISEASES    OF   THE    HEART 

Moreover,  the  loss  of  elasticity  which  these  changes  entail  not 
only  adds  still  further  to  the  work  of  the  left  ventricle,  but  is  also  a 
fertile  source  of  arterial  rupture. 

The  forcible  and  excessive  distension  of  the  peripheral  vessels 
by  the  powerful  systole  of  the  left  ventricle,  followed  by  their  sudden 
collapse  during  diastole,  on  account  of  the  loss  of  support  to  the 
column  of  blood  at  the  aortic  orifice,  gives  rise  to  visible  pulsation 
of  the  arteries  throughout  the  body.  A  peculiar  vermiform  move- 
ment of  the  arterial  tubes  may  also  be  observed  as  the  pulse  wave 
passes  along  it. 

Under  favourable  circumstances  aortic  incompetence  may  endure 
for  many  years  without  giving  rise  to  any  obvious  disturbance  of  the 
systemic  or  pulmonic  circulation. 

Compensation  is  effected  mainly  by  means  of  dilatation  and 
hypertrophy  of  the  left  ventricle.  The  dilatation  of  the  chamber 
affords  accommodation  for  the  additional  quantity  of  blood  received 
from  the  aorta,  while  the  hypertrophy  enables  the  ventricle  to  cope 
with  the  increased  work  required  of  it. 

When  the  excess  of  blood  thrown  into  the  aorta  at  each  systole 
exactly  counterbalances  the  amount  of  backflow  during  diastole, 
compensation  is  perfect.  This  result  is  not  uncommonly  attained, 
but  in  many  instances  compensation  is  less  satisfactory. 

Arterial  ansemia  and  pulmonic  congestion  develop  in  proportion 
to  the  degree  of  cardiac  insufficiency. 

The  salutary  effects  of  hypertrophy  of  the  right  ventricle  and  the 
disastrous  results  which  follow  dilatation  of  this  chamber  from 
failure  have  already  been  mentioned.  The  breakdown  of  compensa- 
tion in  aortic  incompetence  may  be  sudden  or  gradual,  and  is  due 
to  failure  of  the  left  ventricle,  which  undergoes  progressive  dilatation 
from  incomplete  emptying,  in  consequence  of  the  exhaustion  of  its 
muscular  walls  induced  by  long-continued  overwork. 

The  series  of  changes  which  lead  to  the  final  result  follow  one  of 
two  courses.  In  one  event  the  progressive  inadequacy  of  the  left 
ventricle  is  accompanied  by  excessive  arterial  anaemia  and  its 
effects ;  there  is  little  or  no  embarrassment  of  the  pulmonic  cir- 
culation, and  dropsy  is  usually  slight  or  absent.  In  the  other  and 
more  common  event  the  increasing  dilatation  of  the  left  ventricle 
leads  to  relative  incompetence  of  the  mitral  valve  followed  by 
pulmonic  engorgement,  dilatation  of  the  right  heart,  general  venous 
congestion,  and  dropsy. 

Under  either  set  of  conditions  the  over-distension  of  the  left 
ventricle  may  result  in  sudden  arrest  of  the  heart's  action  in  diastole. 

Sudden  death  in  aortic  incompetence  occurs  most  commonly  in 
those  instances  in  which  the  lesion  arises  after  middle  life,  when 
satisfactory  compensation  is  hardly  ever  established. 


AORTIC    INCOMPETENCE  199 

SYMPTOMS 

Aortic  incompetence,  the  result  of  endocarditis,  may  endure  for 
many  years  without  giving  rise  to  symptoms  of  any  importance. 

The  lesion,,  in  cases  of  this  kind,  is  usually  inconsiderable,  and 
the  compensatory  changes  in  the  left  ventricle  are  so  perfect  that  the 
valvular  insufficiency  produces  no  appreciable  disturbance  of  the 
systemic  and  pulmonic  circulations.  It  frequently  happens,  too, 
under  these  circumstances,  that  the  patient  is  able  to  undergo  great 
physical  and  mental  exertion  without  any  obvious  discomfort. 

This  condition  of  affairs  is,  however,  the  exception  rather  than 
the  rule,  and  it  is  usual,  even  in  well-compensated  cases,  to  find  that 
the  subjects  of  aortic  incompetence  suffer  from  undue  shortness  of 
breath  when  any  unusual  effort  is  made.  At  the  same  time,  this 
symptom  is  not  so  pronounced  as  in  mitral  affections,  owing  to  the 
absence  of  pulmonic  congestion  in  the  early  stages  of  aortic  disease. 

A  variable  degree  of  anaemia  is  noticeable  almost  from  the  outset 
in  nearly  all  cases  of  aortic  insufficiency,  and  pallor  becomes  a  very 
marked  feature  of  the  terminal  stages  of  the  disease. 

Epistaxis  is  sometimes  an  early  and  troublesome  symptom,  and 
should,  in  the  absence  of  a  definite  exciting  cause,  suggest  an 
examination  of  the  heart. 

Throbbing  of  the  carotid  arteries  and  other  vessels  is  often  a 
source  of  much  discomfort  to  the  patient. 

Headache,  giddiness,  faintness,  vertigo,  sleeplessness,  noises  in  the 
ears,  and  flashes  of  light  before  the  eyes  are  of  common  occurrence, 
and  depend  upon  disturbance  of  the  cerebral  circulation. 

Prsecordial  pain  may  be  very  severe,  and  attacks  of  true  angina 
pectoris  are  more  frequently  experienced  in  aortic  incompetence 
than  in  any  other  form  of  valvular  disease. 

Evidence  of  the  breakdown  of  compensation  is  shown,  in  the 
majority  of  cases,  by  gradually  increasing  shortness  of  breath,  palpi- 
tation, precordial  pain,  and  irregularity  of  the  heart's  action  in 
association  with  the  signs  and  symptoms  of  pulmonic  engorgement, 
portal  and  systemic  venous  congestion  and  dropsy. 

The  series  of  events  which  lead  up  to  the  fatal  issue  do  not 
always  take  this  course,  for  in  a  considerable  number  of  instances 
the  signs  of  "  backworking "  through  the  mitral  orifice  are  either 
absent  or  but  slightly  marked,  and  the  patient  suffers  chiefly  from 
arterial  ansemia. 

This  group  of  cases  is  characterized  by  syncopal  and  anginoid 
attacks  which  are  commonly  attended  by  irregularity  and  inter- 
mission of  the  heart's  action.  An  attack  of  syncope  sometimes 
terminates  in  sudden  death. 

Dyspnoea  is  easily  excited  and  is  apt  to  come  on  in  paroxysms, 
but  there  is  no  habitual  shortness  of  breath.  Sleeplessness  is  some- 
times a  prominent  and  distressing  symptom,  while  vomiting,  which 
is  not  uncommon,  is  always  a  serious  feature. 


200  DISEASES  OF  THE  HEART 

The  signs  and  symptoms  of  systemic  venous  engorgement  and 
visceral  congestion  are  not  observed,  and  as  a  rule  dropsy  is  slight 
or  altogether  wanting. 

Sudden  death,  from  over-distension  and  paralysis  of  the  left 
ventricle,  is  more  commonly  observed  in  aortic  incompetence  than 
in  any  other  form  of  valvular  disease.  This  occurrence  is  especially 
to  be  feared  in  those  cases  in  which  the  lesion  has  arisen  during  or 
after  middle  life,  when  compensation  is  seldom  or  never  satisfactory. 

Cerebral  haemorrhage  consequent  on  the  rupture  of  a  vessel  is 
also  a  cause  of  rapid  death  in  aortic  incompetence. 

The  occurrence  of  aortic  regurgitation  consequent  on  the  rupture 
of  a  valvular  cusp  is  associated  with  the  feeling  of  something  having 
given  way  in  the  chest,  and  with  sudden  breathlessness  and  prae- 
cordial  anxiety  and  oppression.  The  signs  and  symptoms  of  rapid 
dilatation  of  the  heart  are  subsequently  developed  in  a  greater  or 
less  degree. 

COMPLICATIONS 

The  complications  which  may  arise  in  the  course  of  aortic  incom- 
petence are  to  a  large  extent  similar  to  those  described  in  con- 
nection with  mitral  disease.  The  points  of  distinction  relate  rather 
to  differences  in  intensity  and  in  the  time  of  occurrence  of  the 
various  phenomena  than  to  differences  in  kind. 

Thus  the  signs  of  pulmonic,  portal,  and  systemic  venous  congestion 
are,  as  a  rule,  later  in  their  appearance  and  less  marked  in  their 
effects  in  aortic  than  in  mitral  lesions,  whereas  this  order  of  events 
is  reversed  with  respect  to  the  time  of  occurrence  and  degree  of 
severity  of  systemic  arterial  anaemia. 

Again,  angina  pectoris  is  a  common  complication  of  aortic  in- 
competence, while,  on  the  other  hand,  it  is  very  rarely  observed 
in  association  with  mitral  disease. 

Degeneration  of  the  walls  of  the  blood  vessels,  which  is  an 
important  factor  in  the  production  of  arterial  rupture,  affects  the 
systemic  side  of  the  circulation  in  aortic  insufficiency,  and  the 
pulmonic  in  mitral  affections. 

The  occurrence  of  embolism  is,  comparatively  speaking,  rare  in 
aortic  incompetence.  Sudden  death  is  more  commonly  observed 
in  aortic  incompetence  than  in  other  form  of  valvular  disease. 
This  is  accounted  for  on  the  grounds  that  the  forces  which  lead 
to  over-distension  of  the  left  ventricle  operate  more  powerfully  in 
aortic  insufficiency  than  in  any  other  valvular  affection. 

The  only  other  compHcation  of  aortic  incompetence  to  which 
special  reference  need  be  made  is  the  occasional  occurrence  of 
collapse  of  the  lower  lobe  of  the  left  lung  in  consequence  of  the 
pressure  exerted  upon  it  by  the  enlarged  left  ventricle. 

PHYSICAL  SIGNS 

Physiognomy. — The  face  is  usually  very  pale  or  greyish  white 
in  colour  and  often  wears  a  somewhat  anxious  expression. 


AORTIC   INCOMPETENCE  201 

The  skin  and  mucous  membranes  are  anaemic. 

Pulsation  may  be  observed  in  the  arteries  of  the  neck,  head, 
and  other  parts,  and  is  often  accompanied  by  a  visible  locomotion 
of  the  vessels. 

The  development  of  mitral  regurgitation  in  the  course  of  aortic 
incompetence  may  give  rise  to  some  cyanosis  of  the  lips  and  face, 
but  pallor  usually  predominates  even  under  these  circumstances. 

Pulse. — The  pulse  is  slightly  increased  in  frequency,  but  remains 
regular  in  force  and  rhythm  until  the  heart  fails. 

The  artery  is  large,  but  empty  between  the  beats,  and  the  vessel 
wall  is  usually  more  or  less  thickened  and  tortuous. 

The  pulse  wave  is  sudden,  large,  and  sometimes  vibratory ;  its 
duration  is  very  short ;  it  rises  quickly  and  falls  remarkably  abruptly, 
so  that  it  acquires  the  collapsing  character  so  peculiar  to  the  pulse 
of  aortic  regurgitation.  Hence  the  terms  "collapsing  pulse,"  "water- 
hammer  pulse,"  etc.,  which  have  been  used  to  describe  it. 

So  long  as  the  heart  is  acting  powerfully  the  peculiar  features 
of  the  radial  pulse  are  exaggerated  by  raising  the  arm. 

The  collapsing  character  of  the  pulse  is  often  most  readily 
appreciated  by  grasping  the  fleshy  part  of  the  raised  forearm  of 
the  patient  with  one  or  both  hands. 

Another  feature  of  considerable  interest  with  regard  to  the  pulse 
in  aortic  incompetence  is  the  loss  of  time  manifested  between  the 
systole  of  the  left  ventricle  and  the  appearance  of  the  pulse  wave 
at  the  wrist.  This  phenomenon,  which  is  not  confined  to  the  pulse  of 
aortic  regurgitation,  is  probably  due,  according  to  Professor  AUbutt 
(quoting  Chapman),  to  prolongation  of  the  systole  of  the  left 
ventricle. 

The  collapsing  character  of  the  pulse  is  explained  by  the  rapid 
and  forcible  injection  of  a  much  larger  quantity  of  blood  than 
usual  into  the  aorta  and  systemic  arteries,  and  the  sudden  emptying 
of  these  vessels  in  consequence  'of  the  backward  flow  into  the  left 
ventricle  and  the  onward  flow  into  the  capillaries. 

The  dilatation  of  the  arteries,  like  that  of  the  ventricle,  is  a 
compensatory  change,  since  it  provides  room  for  the  increased 
quantity  of  blood  which  the  systemic  vessels  must  accommodate 
in  order  to  neutralize  the  effects  of  the  regurgitation  through  the 
aortic  orifice. 

The  dilatation  of  the  small  arteries  in  conjunction  with  the 
forcible  action  of  the  hypertrophied  left  ventricle  is  the  source  of 
the  phenomenon  known  as  capillary  pulsation,  which  is  observed  in 
the  skin,  nails,  and  mucous  membranes  in  some  cases  of  aortic 
incompetence.  It  is  due  to  the  failure  of  the  dilated  arteries  to 
obliterate  the  pulse  wave,  which  in  consequence  penetrates  as  far  as 
the  capillaries,  and  in  some  instances  as  far  as  the  peripheral  veins, 
with  the  production  of  venous  pulsation. 

Capillary  pulsation  is  most  readily  elicited  by  gentle  friction  of 


202  DISEASES    OF   THE    HEART 

the  skin  until  it  becomes  reddened,  when  it  will  be  noticed  that  the 
colour  fades  with  each  diastole  and  reappears  with  each  systole 
of  the  heart. 

The  pulsus  bisferiens  is  sometimes  found  in  association  with 
aortic  incompetence. 

Pressure  with  the  stethoscope  over  a  large  artery,  such  as  the 
carotid,  brachial,  or  femoral,  etc.,  sometimes  gives  rise  to  a  to-and- 
fro  murmur  at  the  site  of  constriction,  consequent  on  the  forma- 
tion of  a  fluid  vein,  which  is  produced  not  only  by  the  onward  flow 
during  systole,  but  also  by  the  backward  flow  towards  the  left 
ventricle  during  diastole. 

The  systolic  and  diastolic  elements  of  the  bruit  may  occur 
separately,  and  the  presence  of  the  latter  is  always  significant  of 
extensive  regurgitation  through  the  aortic  orifice. 

HEART 

Inspection. — The  cardiac  impulse  is  diffused,  and  there  is  not 
uncommonly  some  bulging  of  the  prsecordial  region.  The  apex 
beat  is  displaced  downwards  and  outwards.  Systolic  recession  of  the 
intercostal  spaces  in  the  neighbourhood  of  the  apex  beat  is  some- 
times observed. 

Palpation. — The  impulse  of  the  left  ventricle  is  unusually  powerful, 
and  conveys  the  sensation  of  a  forcible  heave  or  thrust.  A  diastolic 
impulse  is  sometimes  felt  at  the  apex  when  the  amount  of  regurgita- 
tion is  excessive,  and  the  left  ventricle  has  undergone  considerable 
dilatation. 

A  diastolic  thrill  is  occasionally  observed  over  the  base  of  the 
heart,  and  in  rare  instances  a  presystolic  thrill  can  be  felt  in  the 
region  of  the  apex. 

Percussion. — The  area  of  cardiac  dulness  is  increased  in  all 
directions,  but  chiefly  downwards  and  to  the  left,  in  correspondence 
with  the  hypertrophy  and  dilatation  of  the  left  ventricle. 

The  right  limit  of  cardiac  dulness  rarely  extends  much  beyond 
the  right  sternal  edge,  and  commonly  lies  within  this  line. 

Auscultation. — At  the  base  of  the  heart,  over  the  aortic  cartilage, 
the  second  sound  is  found  to  be  wholly  or  partially  replaced  by  a 
diastolic  murmur,  which  is  propagated  directly  downwards  along  the 
sternum  as  far  as  the  ensiform  cartilage,  or  obliquely  downwards 
towards  the  apex.  In  the  upward  direction  it  may  be  audible  as 
high  as  the  sterno-clavicular  articulation,  or  even  higher.  The 
murmur  is  usually  soft  and  blowing  in  character,  but  in  some 
instances  it  acquires  a  musical  quality,  while  in  others  it  is  loud, 
rough,  and  vibratory,  It  may  occupy  the  whole  or  a  portion 
only  of  the  diastolic  period,  and  as  a  rule  it  tails  off  towards  its 
termination. 

The  site  of  maximum  intensity  of  the  murmur  varies  in  different 


AORTIC    INCOMPETENCE  203 

cases.  In  some  it  is  heard  best  about  the  mid  sternum,  or  along 
the  left  sternal  edge  between  the  third  and  fifth  ribs ;  in  others  it  is 
loudest  over  the  ensiform  cartilage  or  at  the  apex. 

The  variability  in  the  site  over  which  the  murmur  is  most 
distinctly  audible  depends  mainly  on  differences  in  the  position 
{i.e.  the  particular  cusp  or  cusps  affected),  character,  and  extent 
of  the  valvular  lesion,  whereby  the  direction  of  the  regurgitant 
stream  and  the  vibratile  qualities  of  the  tendinous  structures  com- 
posing the  valve  are  materially  altered. 

The  condition  of  the  aortic  second  sound  requires  careful  investi- 
gation. The  presence  or  absence  of  the  sound  furnishes  important 
evidence  in  the  estimation  of  the  amount  of  regurgitation. 

In  order  to  avoid  the  possibility  of  confusing  the  aortic  with  the 
pulmonic  second  sound  the  stethoscope  should  be  placed  over  the 
carotids  in  the  neck,  where  the  latter  sound  is  inaudible. 

So  long  as  the  aortic  sound  is  heard,  or,  in  other  words,  so  long 
as  the  segments  of  the  valve  are  capable  of  giving  rise  to  audible 
vibrations,  they  must  still  act  as  a  check  to  the  backflow  of  blood 
into  the  left  ventricle,  and  therefore  the  amount  of  regurgitation 
cannot  be  very  great. 

On  the  other  hand,  absence  of  the  aortic  second  sound  is  among 
the  signs  of  serious  leakage. 

The  first  sound  at  the  base  of  the  heart  over  the  aortic  cartilage 
may  be  unaltered,  or  it  may  be  more  or  less  replaced  by  a  systolic 
murmur,  due  to  coexisting  stenosis  of  the  aortic  opening  or  to 
dilatation  of  the  root  of  the  aorta. 

A  systolic  bruit  in  this  situation  may  depend  also  on  ansemia,  on 
roughening  of  the  aortic  cusps,  or  on  aortitis. 

The  differential  diagnosis  of  the  systolic  elemen.;  of  a  combined 
systolic  and  diastolic  murmur,  audible  over  the  aortic  cartilage,  will 
be  considered  under  aortic  stenosis. 

At  the  apex  the  first  sound  is  usually  somewhat  dull  and  muffled, 
and  it  may  be  accompanied  by  a  systolic  bruit,  which  is  due  either 
to  the  muscular  and  relative  incompetence  of  the  mitral  valve, 
attending  dilatation  of  the  left  ventricle,  or  to  concurrent  structural 
disease  at  this  orifice. 

The  diastolic  murmur  is  not  uncommonly  audible  at  the  apex, 
and  in  some  instances  it  so  closely  simulates  the  presystolic  bruit, 
observed  in  cases  of  mitral  stenosis,  that  the  exclusion  of  the  latter 
lesion  is  almost  impossible. 

The  cause  of  the  phenomenon  in  aortic  incompetence  is  still  a 
matter  of  doubt,  but  it  has  been  explained  by  supposing  that  the 
large  anterior  flap  of  the  mitral  valve  is  thrown  into  vibration  either 
by  the  two  blood  currents  which  flow  against  its  opposite  sides,  or 
by  the  direct  impact  of  the  regurgitant  stream  from  the  aorta. 
Another  view  (that  of  Flint)  suggests  that  the  rapid  filling  of  the 
left  ventricle  from  two  sources  floats  up  the  mitral  curtains,  so  that 
at  the  time  of  the  auricular  systole  there  is  a  virtual  stenosis  of  the 


204  DISEASES    OF   THE    HEART 

mitral  orifice,  and  the  current  of  blood  flowing  between  the  opposed 
segments  of  the  valve,  throws  them  into  vibrations,  whereby  the 
characteristic  murmur  is  produced. 

In  whatever  manner  produced,  the  presence  of  a  presystolic  thrill 
and  bruit  at  the  apex,  in  association  with  well-marked  signs  of  aortic 
incompetence,  is  by  no  means  conclusive  of  the  coexistence  of 
mitral  narrowing.  In  cases  of  this  kind  the  diagnosis  of  mitral 
stenosis  must  be  based  on  a  careful  consideration  of  the  concomitant 
signs  and  symptoms  of  the  condition. 


DIAGNOSIS 

The  diagnosis  of  aortic  incompetence  seldom  gives  rise  to  much 
difficulty,  and  depends  chiefly  on  the  association  of  an  aortic 
diastolic  murmur  with  enlargement  of  the  left  ventricle  and  a  col- 
lapsing pulse. 

In  the  absence  of  the  diastolic  murmur,  an  event  of  very  rare 
occurrence,  the  peculiar  characters  of  the  pulse  and  the  alteration 
in  size  of  the  left  ventricle  would  suffice  for  the  recognition  of  the 
lesion. 

The  site  of  maximum  intensity  and  the  area  of  distribution  of 
the  bruit,  taken  in  conjunction  with  the  concomitant  changes  in  the 
heart  and  pulse,  serve  to  distinguish  it  from  diastolic  murmurs  pro- 
duced in  other  situations. 

The  differential  diagnosis  of  the  nature  of  the  lesion  lies  for  the 
most  part  between  endocarditis  and  atheromatous  disease,  since, 
in  the  large  majority  of  cases,  aortic  incompetence,  whether  it 
occurs  alone  or  in  combination  with  stenosis,  is  due  to  the  one 
or  to  the  other  of  these  morbid  processes.  In  attempting  to  dis- 
tinguish between  them,  the  age,  sex,  occupation,  and  history  of 
the  patient,  as  well  as  the  associated  symptoms  and  physical  signs, 
must  be  taken  into  consideration. 

In  young  people  and  women,  and  especially  in  those  cases  in 
which  there  is  a  definite  history  of  acute  or  chronic  rheumatism, 
the  probabilities  are  greatly  in  favour  of  endocarditis. 

On  the  other  hand,  if  the  subject  is  a  man  of  middle  age,  in 
whom  there  is  evidence  of  overwork,  strain,  gout,  syphilis,  alcohol- 
ism, chronic  renal  disease,  etc.,  and  no  history  of  rheumatism,  the 
lesion  may  reasonably  be  ascribed  to  atheroma. 

The  differentiation  between  the  two  forms  of  disease  producing 
aortic  incompetence  is,  however,  more  accurately  and  certainly 
made  by  means  of  the  physical  signs. 

Thus  the  pulse  of  aortic  regurgitation  due  to  atheromatous  disease 
of  the  aortic  valve  shows  little  or  no  real  collapse  of  the  artery 
between  the  beats.  The  vessel  is  large,  firm,  and  tortuous,  and  its 
walls  are  more  or  less  thickened.     The  pulse  wave  comes  and  goes 


AORTIC    INCOMPETENCE  205 

quickly,  and  though  easily  compressible,  the  artery  can  commonly 
be  felt  between  the  beats. 

The  absence  of  collapse  in  the  pulse  is  accounted  for  by  the 
comparatively  small  amount  of  regurgitation  which  of  necessity 
must  obtain  in  atheromatous  affections  of  the  aortic  valve,  since  any 
large  amount  of  valvular  insufficiency  from  this  cause  would  be 
incompatible  with  life. 

Furthermore,  the  retardation  of  the  pulse  wave  between  the  heart 
and  peripheral  arteries  is  much  less  marked  in  aortic  incompetence 
due  to  atheroma  than  in  that  caused  by  endocarditis. 

As  regards  the  cardiac  physical  signs,  it  may  be  noted  that  while  a 
combined  murmur  {i.e.  systolic  and  diastolic)  may  occur  in  both 
forms  of  the  disease,  it  is  more  commonly  found  in  association  with 
atheromatous  than  with  inflammatory  affections  of  the  aortic  valve. 

Of  much  greater  importance,  however,  is  the  character  of  the 
aortic  second  sound.  As  already  pointed  out,  this  sound  is  impaired 
or  lost  in  that  form  of  valvular  insufficiency  which  is  produced  by 
endocarditis.  In  atheromatous  lesions  at  the  aortic  opening  accom- 
panied by  incompetence  of  the  valve,  the  second  sound  is  often 
loud  and  ringing  in  quality,  and  is  heard  immediately  in  front  of  the 
diastolic  bruit. 

The  presence  of  the  symptoms  or  signs  of  dilatation  or  aneurism 
of  the  aorta,  in  addition  to  those  of  aortic  incompetence,  would 
afford  strong  evidence  in  favour  of  an  atheromatous  lesion.  Attacks 
of  cardiac  pain  or  angina  pectoris  disproportionate  to  the  severity 
of  the  lesion,  estimated  on  other  grounds,  would  point  in  the  same 
direction. 

It  must,  however,  be  borne  in  mind  that  the  two  forms  of  disease 
may  coexist,  for,  in  many  instances,  a  lesion  originally  due  to  endo- 
carditis becomes  the  seat  of  atheromatous  changes  and  vice  versa. 
In  this  way  a  differential  diagnosis  may  be  rendered  impossible. 


THE  ESTIMATION  OF  THE  AMOUNT  OF   BACKFLOW 
IN  AORTIC  INCOMPETENCE 

The  following  are  the  chief  sources  of  information : — 

I.  The  character  of  the  imlse, — The  suddenness,  rapidity,  and 
extent  of  the  arterial  collapse,  the  size  of  the  vessel,  and  its  con- 
dition between  the  beats  are  the  points  to  which  attention  should 
be  chiefly  directed. 

If  the  artery  is  emptied  gradually,  and  especially  if  it  can  be  felt 
between  the  beats,  and  is  of  moderate  size,  the  amount  of  regurgita- 
tion is  inconsiderable,  even  though  the  pulse  wave  be  sudden  and 
forcible. 

The  more  rapid  and  complete  the  collapse  of  the  pulse  the  greater 
is  the  amount  of  regurgitation. 

Among  the  other  indications  of  severe  incompetence  are  well- 


2o6  DISEASES   OF  THE   HEART 

marked  capillary  or  venous  pulsation,  and  the  presence  of  a  diastolic 
murmur  in  the  peripheral  arteries. 

A  visible  pulse  in  the  superficial  peripheral  arteries  such  as  the 
carotids,  radials,  etc.,  invariably  accompanies  serious  insufficiency 
of  the  aortic  valve,  provided  the  left  ventricle  is  not  failing. 

2.  The  extent  and  character  of  the  enlargement  of  the  left 
ventricle. — In  the  absence  of  the  symptoms  or  signs  of  circulatory 
embarrassment  the  degree  of  hypertrophy  and  dilatation  of  the  left 
ventricle  is,  to  a  large  extent,  a  measure  of  the  severity  of  the 
valvular  incompetence. 

If  the  heart  is  failing,  hypertrophy  has  more  significance  than 
dilatation,  but  it  cannot  be  said  that  either  condition  has  much 
weight  in  the  estimation  of  the  amount  of  regurgitation  under  these 
circumstances. 

3.  The  presence  or  absence  of  the  second  sound  in  the  neck. — 
If  the  second  sound  is  audible  over  the  carotid  arteries  in  the  neck, 
it  follows,  for  the  reasons  previously  given,  that  the  amount  of  back- 
flow  into  the  left  ventricle  cannot  be  large.  On  the  other  hand,  the 
absence  of  the  second  sound  in  this  situation  is  one  of  the  signs 
of  serious  incompetence. 

4.  The  character  of  the  murmur. — The  information  afforded  by 
the  character  of  the  murmur  is  of  very  little  value. 

As  a  rule,  a  loud  murmur  signifies  that  the  heart  is  acting  with 
vigour,  and  therefore  the  probabilities  are  that  the  amount  of  leakage 
is  not  very  great. 

Severe  incompetence  may  be  associated  with  a  short,  soft,  diastolic 
bruit. 


CHAPTER    XIV 
AORTIC    STENOSIS 

Pathogenesis — Morbid  Anatomy — Effects  on  the  Heart  and  Circulation — Compen-  ' 
sation  :  its  duration  and  failure — Symptoms — Complications — Mode  of  Termi- 
nation— Physical  Signs — Diagnosis — Estimation  of  degree  of  Stenosis. 

iETIOLOGICAL  PATHOLOGY 

Aortic  stenosis  arises  under  precisely  the  same  pathological  con- 
ditions as  aortic  incompetence.  The  chief  causes,  therefore,  of 
aortic  stenosis  are  :  (i)  endocarditis  due  to  rheumatism,  the  zymotic 
fevers,  syphilis,  etc. ;  (2)  endocarditis  due  to  prolonged  muscular 
strain ;  (3)  atheroma  which  may  attack  the  aortic  valve  primarily, 
or,  as  most  commonly  happens,  by  extension  from  the  aorta. 

Aortic  stenosis  is  occasionally  observed  as  a  congenital  mal- 
formation. 

The  morbid  changes  lead  to  thickening,  rigidity,  and  retraction 
of  the  semilunar  cusps,  with  more  or  less  induration  and  constriction 
of  the  fibrous  aortic  ring. 

The  segments  of  the  valve  sometimes  become  adherent  to  one 
another,  and  thus  diminish  the  size  of  the  orifice,  or  they  may  be 
the  seat  of  abundant  vegetations,  which  obstruct  the  passage  of 
blood  through  the  opening. 

Atheromatous  disease  of  the  valve  sometimes  leads  to  more  or 
less  complete  calcification  of  the  semilunar  cusps  and  basal  ring. 
The  cusps  of  the  valve  are  consequently  unable  to  fall  back  com- 
pletely during  the  ventricular  systole,  so  that  a  variable  degree  of 
obstruction  is  produced  at  the  aortic  opening. 

In  a  very  large  proportion  of  cases  aortic  stenosis  is  combined 
with  incompetence  of  the  valve,  owing  to  the  inability  of  the 
thickened  and  rigid  segments  to  adequately  close  the  narrowed 
orifice. 

Indeed,  pure  aortic  obstruction  is  one  of  the  rarest  of  cardiac 
lesions,  but  it  will  be  convenient  to  include  in  this  description  those 
forms  of  aortic  disease  in  which  stenosis  is  the  predominant  feature. 


2o8  DISEASES   OF   THE   HEART 

PATHOLOGICAL    RESULTS 
Effects  on  the  Heart  and  Circulation 

The  effect  of  aortic  stenosis  is  to  interfere  with  the  passage  of 
blood  from  the  left  ventricle  into  the  aorta  during  systole. 

The  difficulty  experienced  by  the  left  ventricle  in  the  expulsion 
of  its  contents  calls  for  an  increased  display  of  force,  which,  under 
favourable  circumstances,  leads  to  hypertrophy  of  its  walls.  If,  by 
this  means,  the  volume  of  blood  propelled  into  the  aorta  during 
each  systole  does  not  fall  below  the  normal,  compensation  is  estab- 
lished. It  will  therefore  appear  that  in  aortic  stenosis  compensa- 
tion depends  solely  on  hypertrophy  of  the  left  ventricle. 

If  the  constriction  of  the  opening  is  attended  by  incompetence  of 
the  valve,  a  variable  degree  of  dilatation  of  the  left  ventricle  is  also 
produced,  for  the  reasons  which  were  given  in  the  previous  chapter. 

Uncomphcated  aortic  stenosis  may  endure  for  many  years  without 
giving  rise  to  any  appreciable  disturbance  of  the  circulation  ;  indeed, 
it  sometimes  happens  that  the  lesion  is  not  discovered  until  after 
death  from  other  causes. 

Compensation  is  maintained  longer  in  aortic  stenosis  than  in  any 
other  form  of  valvular  disease,  but  in  the  absence  of  a  definite 
exciting  cause  failure  of  the  heart  is  rarely  recovered  from. 

The  breakdown  of  compensation  usually  depends  on  progressive 
constriction  of  the  aortic  orifice,  or  on  interference  with  the  blood 
supply  to  the  heart  through  the  coronary  arteries,  or  on  the  occur- 
rence of  a  comphcation. 

The  left  ventricle  becomes  unable  to  completely  empty  itself  at 
each  systole,  and  consequently  undergoes  dilatation  from  incomplete 
emptying,  i.e.  from  failure. 

A  variable  degree  of  arterial  anaemia  ensues,  and  the  dilatation  ot 
the  left  ventricle,  if  continued,  leads  to  muscular  and  relative  in- 
competence of  the  mitral  valve,  followed  by  pulmonic  engorgement, 
dilatation  of  the  right  heart,  general  venous  congestion,  and  dropsy. 

The  occurrence  of  mitral  regurgitation  in  the  course  of  aortic 
stenosis  may  depend  also  on  chronic  forcing  of  the  mitral  valve  by 
the  high  pressure  which  prevails  in  the  left  ventricle,  or  on  con- 
comitant structural  disease  at  the  mitral  orifice. 


SYMPTOMS 

So  long  as  compensation  is  good,  the  subjects  of  aortic  stenosis 
remain  free  from  symptoms  until  the  degree  of  narrowing  becomes 
sufficiently  great  to  seriously  interfere  with  the  supply  of  blood  to 
the  aorta  and  systemic  vessels.  The  patient  then  begins  to  suffer 
from  headache,  giddiness,  syncopal  attacks,  and  other  symptoms  of 
disordered  cerebral  circulation. 


AORTIC   STENOSIS  209 

Anccmia  is  developed,  and  the  defective  supply  of  blood  to  the 
systemic  arteries  leads  to  interference  with  nutrition  and  coldness  of 
the  extremities  associated  with  general  nervous  and  muscular  debility^^^ 

As  compensation  begins  to  fail,  dyspnoea,  palpitation,  pain,  which 
may  have  anginal  characters,  and  other  symptoms  of  cardiac  in- 
sufficiency make  their  appearance. 

The  dilatation  of  the  left  ventricle  which  accompanies  failure  of 
compensation  is  attended  by  regurgitation  through  the  mitral  orifice, 
together  with  the  signs  and  symptoms  of  pulmonic  and  systemic 
venous  congestion. 

As  a  rule  death  takes  place  slowly  from  gradual  failure  of  the 
ventricles.  A  sudden  termination  is  sometimes  observed  as  the 
result  of  syncope,  embolism,  or  the  rupture  of  a  cerebral  vessel. 

The  complications  of  aortic  stenosis  do  not  require  special  con- 
sideration, since  they  resemble,  for  the  most  part,  those  described  in 
connection  with  aortic  incompetence. 

PHYSICAL  SIGNS 

Physiognomy. — The  appearance  presented  by  the  subjects  of 
aortic  stenosis  is  in  no  way  characteristic  until  the  disease  has  made 
considerable  progress,  when  the  signs  of  ansemia  are  gradually 
developed.  The  complexion  then  acquires  the  sallow  or  greyish- 
white  hue  described  under  aortic  regurgitation,  and  the  skin  and 
mucous  membranes  become  pallid. 

A  bluish  tinge  affecting  the  lips,  cheeks,  and  extremities,  etc., 
may  be  noticed  after  failure  of  the  left  ventricle  has  occurred,  and 
is  due  to  insufficient  aeration  of  the  blood  following  leakage  through 
the  mitral  valve  and  the  consequent  production  of  pulmonic  con- 
gestion. 

Pulse. — So  long  as  compensation  is  maintained  the  pulse  is  slow 
and  regular  both  in  force  and  frequency.  The  artery  is  small  and 
can  be  felt  between  the  beats,  but,  as  a  rule,  is  easily  compressible. 

The  pulse  wave  is  small,  long,  and  well  sustained ;  it  rises  gradu- 
ally and  falls  slowly. 

Both  the  anacrotic  and  the  bisferiens  pulse  may  be  found  in 
association  with  aortic  stenosis,  but  it  cannot  be  said  that  either 
pulse  is  pathognomonic  of  this  lesion. 

The  exact  significance  of  these  pulses  has  not  yet  been  fully 
worked  out,  but,  speaking  generally,  the  indication  in  either  event 
is  organic  disease  at  the  orifice  or  along  the  course  of  the  aorta. 

HEART 

Inspection. — Bulging  of  the  prsecordial  region  is  not  uncommon. 
The  apex  beat  is  displaced  downwards  and  slightly  outwards. 

Palpation. — -The   impulse    of  the   left   ventricle   conveys   to   the 
hand  the  impression  of  a  slow,  deliberate,  forcible  thrust.     A  thrill, 
systolic  in  time,  is  sometimes  palpable  over  the  base  of  the  heart. 
p 


2IO  DISEASES  OF  THE  HEART 

Percussion. — The  area  of  cardiac  dulness  is  increased  chiefly 
downwards  and  to  the  left,  and  corresponds  with  the  enlargement 
of  the  left  ventricle. 

Auscultation. — At  the  base  of  the  heart,  over  the  aortic  cartilage, 
the  first  sound  is  accompanied,  or  more  or  less  replaced,  by  a  loud, 
rough,  and  rasping  murmur,  which  is  conducted  upwards  along  the 
right  sternal  edge  into  the  neck.  The  murmur  is  usually  audible 
over  the  upper  portion  of  the  thorax  and  along  the  course  of  both 
carotid  arteries.  It  can  frequently  be  heard  at  the  apex,  and  occa- 
sionally over  the  whole  praecordium. 

The  murmur  usually  has  the  characters  above  indicated,  but  in 
some  instances  it  is  soft  and  blowing,  in  others  musical. 

As  a  rule  the  bruit  occupies  the  whole  of  the  interval  between  the 
commencement  of  the  first  sound  and  the  occurrence  of  the  second 
sound.  The  second  sound  over  the  aortic  cartilage  is  commonly 
muffled  and  indistinct,  and  is  sometimes  more  or  less  replaced  by  a 
diastolic  murmur. 

The  first  sound  at  the  apex  is  usually  dull  and  ill  defined,  and  may 
be  accompanied  by  a  systolic  bruit  of  mitral  origin. 

The  establishment  of  mitral  regurgitation,  which,  as  already  ex- 
plained, takes  place  sooner  or  later  in  the  course  of  aortic  stenosis, 
is  followed  by  the  signs  and  symptoms  of  pulmonic  engorgement, 
portal  and  systemic  venous  congestion,  and  dropsy. 

The  occurrence  of  this  train  of  events  in  association  with  aortic 
stenosis,  in  the  absence  of  a  definite  existing  cause,  indicates  failure 
of  the  left  ventricle  and  the  breakdown  of  compensation,  and  is 
usually  of  the  worst  possible  augury. 

DIAGNOSIS 

In  the  diagnosis  of  aortic  stenosis  much  more  importance  attaches 
to  the  character  of  the  pulse  and  to  the  changes  in  the  left  ventricle 
than  to  the  presence  of  a  systolic  murmur  in  the  aortic  area,  inas- 
much as  the  latter  sign  may  be  observed  in  various  other  conditions, 
chief  among  which  are  rigidity,  roughening,  or  fenestration  of  one 
or  more  of  the  cusps  of  the  aortic  valve,  dilatation  or  aneurism  of 
the  aorta,  anjemia,  and  acute  or  sub-acute  aortitis. 

A  systolic  basic  murmur,  due  to  the  roughening  and  rigidity  of  the 
aortic  cusps,  that  is  caused  by  atheroma  is  almost  certainly  ac- 
companied by  accentuation  of  the  second  sound,  and  is  therefore 
not  likely  to  be  mistaken  for  the  bruit  of  aortic  stenosis.  Again, 
fenestration  of  an  aortic  cusp,  or  a  shred  of  fibrin  hanging  from 
some  portion  of  the  valve,  would  not  give  rise  to  any  modification  of 
the  pulse,  or  to  enlargement  of  the  left  ventricle. 

In  dilatation  of  the  aorta  the  volume  of  the  pulse  is  larger  than  in 
aortic  stenosis.  Moreover,  the  presence  of  pulsation  and  dulness  in 
the  intercostal  spaces  to  the  right  of  the  sternum  above  the  level 
of  the  third  or  second  rib,  together  with  the  well-marked  and  charac- 


AORTIC  STENOSIS  211 

teristic  accentuation  of  the  second  sound,  which  is  invariably  ob- 
served in  aortic  dilatation  so  long  as  the  aortic  valve  is  competent, 
would  suffice  for  the  recognition  of  the  lesion. 

The  presence  of  pressure  signs  would  establish  the  diagnosis  of 
aortic  aneurism. 

The  systolic  aortic  murmur  due  to  ansemia  is  soft  and  blowing  in 
character,  and  does  not  substitute  itself  for  the  first  sound,  as  in 
aortic  stenosis.  Moreover,  the  murmur  in  the  aortic  area  is  usually, 
if  not  always,  preceded  and  accompanied  by  a  venous  hum  in  the 
neck  and  a  systolic  bruit  in  the  pulmonic  area.  Furthermore,  the 
age  and  general  condition  of  the  patient,  together  with  the  absence 
of  the  signs  of  cardiac  hypertrophy,  or  of  any  special  modification 
in  the  volume  of  the  pulse,  renders  the  differential  diagnosis  be- 
tween anaemia  and  aortic  obstruction  comparatively  easy. 

The  determination  of  the  nature  of  the  lesion  producing  aortic 
stenosis  depends  on  the  age,  sex,  and  history  of  the  patient,  and  on 
the  condition  of  the  peripheral  vessels.  The  cardiac  physical  signs 
do  not,  as  a  rule,  afford  much  information  in  this  respect,  though 
Constantin  Paul  considers  that  the  systolic  bruit  of  aortic  obstruc- 
tion due  to  atheroma  tends  to  spread  laterally  rather  than  vertically. 

If  the  obstruction  at  the  aortic  opening  caused  by  atheroma  is 
due  merely  to  rigidity  of  the  segments  of  the  valve,  the  second  sound 
is  usually  accentuated. 

The  appearance  of  an  aortic  systolic  murmur  accompanied  by 
irregular  pyrexia,  retrosternal  pain  and  rapid  cardiac  failure  would 
be  strongly  suggestive  of  aortitis. 

ESTIMATION  OF  THE  DEGREE  OF  NARROWING 
IN  AORTIC  STENOSIS 

The  degree  of  constriction  in  aortic  stenosis  is  determined  by 
means  of  the  character  of  the  pulse,  and  the  extent  of  the  hyper- 
trophy of  the  left  ventricle. 

1.  The  pulse. — A  moderate  degree  of  arterial  constriction  with  a 
pulse  of  fair  size  is  compatible  with  an  inconsiderable  amount  of 
narrowing  at  the  aortic  orifice.  This  inference  is  strengthened  if  it 
is  found  that  a  sudden  additional  strain  thrown  on  the  heart  leads 
merely  to  increased  force  and  frequency  of  the  pulse. 

On  the  other  hand,  a  small  vessel  with  great  diminution  in  the 
volume  of  the  pulse  is  indicative  of  severe  aortic  obstruction. 

2.  The  degree  of  hypertrophy  of  the  left  ventricle. — So  long  as 
compensation  is  maintained,  the  extent  of  the  ventricular  hyper- 
trophy is  a  measure  of  the  degree  of  stenosis  which  obtains.  Never- 
theless it  cannot  be  too  strongly  insisted  upon  that  the  indications 
afforded  by  the  pulse  altogether  outweigh  the  evidence  supplied  by 
the  condition  of  the  left  ventricle  in  estimating  the  degree  of 
narrowing  in  cases  of  aortic  stenosis. 


CHAPTER   XV 
TRICUSPID    INCOMPETENCE 


Pathogenesis — Morbid    Anatomy — Effects    on    the    Heart    and    Circulation- 
Symptoms — Physical  Signs — Diagnosis— Estimation   of  the   amount   of   Re- 
gurgitation. 

iETIOLOGICAL  PATHOLOGY 

Regurgitation  through  the  tricuspid  opening  may  be  due  to — 

1.  Organic  disease  of  the  segments  of  the  valve 

2.  Muscular  or  relative  incompetence  of  the  valve 

Tricuspid  insufficiency  due  to  structural  disease  of  the  valve  is 
of  comparatively  rare  occurrence.  It  may  be  produced  by  acute, 
sub-acute,  or  chronic  endocarditis,  arising  either  "in  utero"  or  during 
after  life.  In  some  instances  the  insufficiency  of  the  valve  is  due 
to  degenerative  processes. 

The  valvular  incompetence  is  brought  about  by  changes  similar 
to  those  described  in  connection  with  mitral  regurgitation,  and  in 
the  large  majority  of  cases  the  affection  of  the  tricuspid  valve  is 
secondary  to  endocarditis  on  the  left  side  of  the  heart. 

Byrom  Bramwell  is  of  the  opinion  that  acute  inflammation  of  the 
tricuspid  valve  is  much  more  common  than  is  generally  supposed, 
and,  furthermore,  that  the  inflammatory  process  usually  subsides 
without  giving  rise  to  any  permanent  structural  changes. 

Relative  incompetence  of  the  tricuspid  valve  is  primarily  depen- 
dent on  dilatation  of  the  right  ventricle,  the  result  of  the  myocar- 
dial debility  and  degeneration  associated  with  cardiac  overstrain, 
ansemia,  the  acute  specific  fevers,  and  malnutrition  from  other 
causes. 

It  is  observed,  therefore,  in  connection  with  affections  of  the 
pulmonic  valve.  It  is  also  a  common  sequel  to  lesions  of  the  mitral 
valve,  and  sooner  or  later  it  arises  in  all  forms  of  lung  disease 
which  lead  to  obstruction  in  the  pulmonic  circulation. 

The  mechanism  of  production  of  this  form  of  valvular  incom- 
petence has  already  been  fully  considered  in  connection  with  mitral 
regurgitation. 

212 


TRICUSPID    INCOMPETENCE  213 

PATHOLOGICAL   RESULTS 
Effects  on  the   Heart  and   Circulation 

In  consequence  of  the  incomplete  closure  of  the  tricuspid  valve, 
blood  is  forced  backwards  into  the  right  auricle  during  the 
ventricular  systole.  The  auricle,  now  supplied  from  two  sources, 
undergoes  dilatation  from  overfilling  and  its  walls  subsequently 
hypertrophy,  owing  to  the  additional  work  entailed  in  the  pro- 
pulsion of  a  larger  quantity  of  blood  than  usual.  The  latter 
process  is  seldom  very  pronounced,  partly  because  the  auricular 
walls  are  incapable  of  much  hypertrophy,  and  partly  because  the 
conditions  necessary  for  the  development  of  hypertrophy  are  rarely 
satisfactory  in  cases  of  tricuspid  incompetence. 

As  the  result  of  the  increase  in  the  capacity  of  the  right  auricle,  a 
larger  quantity  of  blood  than  normal  is  propelled  into  the  right  ven- 
tricle during  diastole.  Dilatation  of  the  right  ventricle  from  overfilling 
is  thereby  produced,  and  this  process,  in  an  uncomplicated  case  of 
tricuspid  regurgitation,  is  followed  by  hypertrophy  of  the  chamber 
from  increased  work.  Since  in  the  large  majority  of  instances,  how- 
ever, the  limits  of  hypertrophy  have  already  been  reached,  the  former 
effect  alone  is  usually  observed. 

The  high  pressure  which  prevails  in  the  right  auricle,  especially 
during  the  ventricular  systole,  offers  a  serious  obstacle  to  the  return 
of  blood  to  the  heart,  so  that  congestion  and  ultimately  engorge- 
ment of  the  portal  and  systemic  venous  circulations  is  produced. 
Moreover,  the  great  venous  trunks  are  exposed  to  the  direct  effects 
of  the  regurgitant  stream  from  the  ventricle,  which  not  only  inten- 
sifies the  congestion,  but  leads  also  to  distension  and  dilatation  of 
these  vessels. 

It  will  be  unnecessary  to  discuss  here  the  effects  of  portal  and 
systemic  engorgement  on  the  abdominal  and  other  viscera  and 
peripheral  tissues,  inasmuch  as  they  were  fully  considered  in  con- 
nection with  mitral  incompetence. 

It  may,  however,  be  again  pointed  out  that  hepatic  enlargement 
is  an  early  and  characteristic  feature  of  tricuspid  regurgitation. 

Incompetence  of  the  tricuspid  valve  is  also  accompanied  by 
a  greater  or  less  degree  of  arterial  anaemia  consequent  on  the 
diminished  supply  of  blood  to  the  lungs,  and  hence  to  the  left 
heart  and  aorta. 

SYMPTOMS 

In  uncomplicated  cases  regurgitation  through  the  tricuspid  orifice 
may  be  unattended  by  symptoms  of  any  moment,  provided  the 
amount  of  leakage  is  very  slight.  Any  considerable  degree  of 
tricuspid  insufficiency  gives  rise   to  symptoms  which  are  similar. 


214  DISEASES   OF   THE    HEART 

for  the  most  part,  to  those  described  in  connection  with  the  final 
stages  of  mitral  disease. 

The  onset  of  tricuspid  regurgitation  during  the  course  of  left- 
sided  cardiac  lesions  is  evidenced  by  an  increase  of  dyspnoea,  by 
cyanosis  and  dropsy,  and  by  the  symptoms  significant  of  visceral 
engorgement. 

The  shortness  of  breath  is  usually  a  prominent  symptom,  and  is 
aggravated  by  the  occurrence  of  pulmonic  complications,  of  which 
hydrothorax  and  bronchial  catarrh  are  the  most  important. 

Dropsy  commences  with  oedema  of  the  feet  and  ankles  and 
gradually  spreads  upwards.  In  severe  cases  the  serous  cavities, 
as  well  as  all  the  subcutaneous  tissues,  are  involved,  so  that  the 
patient  becomes  more  or  less  completely  waterlogged. 

The  congestion  of  the  portal  circulation  is  shown  by  a  feeling 
of  weight,  heaviness,  or  tenderness  in  the  right  hypochondrium, 
by  digestive  disturbances,  and  by  irregular  action  of  the  bowels. 
Haematemesis  and  melsena  occasionally  occur,  and  are  attributable 
to  the  high  pressure  in  the  portal  vessels. 

Headache,  giddiness,  vertigo,  and  insomnia  are  among  the  indica- 
tions of  the  disturbance  of  the  circulation  through  the  brain. 

The  urine  is  scanty,  high  coloured,  and  usually  throws  down, 
on  cooling,  a  copious  deposit  of  lithates.  It  usually  contains  also 
a  small  quantity  of  albumen,  and  occasionally  a  little  blood. 

Venous  thrombosis  may  lead  to  embolism  of  the  pulmonic  artery, 
and  in  this  way  to  sudden  death.  The  usual  mode  of  termination 
of  these  cases  is  by  gradual  failure  of  the  right  ventricle. 

In  those  instances  in  which  tricuspid  incompetence  is  due  to 
a  temporary  or  curable  cause,  such  as  cardiac  overstrain,  ansemia, 
the  acute  specific  fevers,  etc.,  the  symptoms  do  not  necessarily 
present  the  serious  characters  described  above. 

PHYSICAL  SIGNS 

Physiognomy. — The  subjects  of  tricuspid  incompetence  present 
appearances  similar  to  those  observed  in  the  terminal  stages  of 
mitral  disease.  Thus  the  face  is  dusky  or  livid,  the  lips  become 
cyanosed,  and  the  limbs  and  trunk  are  more  or  less  oedematous. 

In  other  instances  the  signs  of  anaemia  are  obtrusive,  but  in  any 
event  dropsy  is  usually  an  early  and  prominent  feature. 

Pulse. — ^Tricuspid  incompetence,  per  se,  produces  little  alteration 
in  the  character  of  the  pulse.  The  modifications  which  may  be 
observed  are  due,  for  the  most  part,  to  the  lesions  on  the  left  side 
of  the  heart,  whereon  the  tricuspid  affection  depends. 

With  this  reservation,  it  may  be  stated  that  the  pulse  in  tricuspid 
incompetence  is  diminished  in  volume  and  is  usually  irregular  both 
in  force  and  frequency. 

The  artery  is  small  and  cannot  be  felt  between  the  beats,  while 
the  pulse  wave  is  short,  weak,  and  badly  sustained. 


TRICUSPID  INCOMPETENCE  215 

A  reduction  in  the  size  of  the  right  radial  pulse  as  compared  with 
the  left  has  been  observed,  and  is  explained  on  the  assumption  that 
pressure  is  exerted  on  the  right  subclavian  artery  by  the  distended 
right  auricle  and  enlarged  veins. 

HEART 

Inspection. — Examination  of  the  neck  shows  more  or  less  disten- 
sion of  the  jugular  veins,  which  will  frequently  fill  from  the  cardiac 
side  when  emptied  by  pressure  with  the  finger  from  below  upwards. 

Pulsation  is  also  usually  observed  in  the  jugular  veins  when  the 
amount  of  regurgitation  is  considerable.  The  pulsation  is  com- 
monly systolic,  and  is  due  to  the  reflux  wave  along  the  jugulars 
that  is  produced  by  the  ventricular  contraction.  In  some  instances 
the  auricular  contraction  also  gives  rise  to  a  refluent  current  along 
the  veins,  so  that  a  double  jugular  pulsation  {i.e.  presystolic  and 
systolic)  is  observed.  It  must  be  borne  in  mind,  however,  that  jugular 
pulsation  is  not  pathognomonic  of  tricuspid  incompetence,  nor  is 
the  presence  of  the  lesion  excluded  by  the  absence  of  the  sign. 

The  regurgitant  stream  through  the  tricuspid  orifice  is  likewise 
transmitted  into  the  liver,  by  way  of  the  right  auricle,  inferior  vena 
cava,  and  hepatic  veins,  with  the  result  that  systolic  expansile  pul- 
sation of  this  organ  may  also  be  produced. 

Epigastric  pulsation  is  usually  well  marked,  and  is  due  to  the 
movements  of  the  enlarged  right  ventricle. 

Pulsation  is  less  commonly  seen  in  the  third  and  fourth  right 
intercostal  spaces  close  to  the  sternum.  This  sometimes  depends 
on  the  contraction  of  the  right  auricle,  but  in  the  majority  of  cases 
it  is  produced  by  the  refluent  current  from  the  ventricle  into  the 
auricle. 

Palpation. — The  epigastric  impulse  is  forcible  and  heaving  until 
the  right  ventricle  fails. 

Pulsation  may  be  detected  over  the  liver.  Care  must  be  taken, 
however,  not  to  mistake  the  impulse  communicated  to  the  liver 
by  the  systole  of  the  right  ventricle  for  true  hepatic  pulsation. 

Percussion. — The  area  of  cardiac  dulness  is  increased,  especially 
towards  the  right,  in  consequence  of  the  enlargement  of  the  right 
auricle  and  ventricle. 

Extension  of  dulness  to  the  left  is  also  commonly  observed  as 
the  result  of  concurrent  disease  on  the  left  side  of  the  heart. 

The  lower  limit  of  hepatic  dulness  may  extend  down  to,  or  even 
below,  the  level  of  the  umbilicus. 

Auscultation. — Tricuspid  incompetence  is  commonly  attended 
by  a  soft  and  blowing  systolic  murmur,  which  partially  or  wholly 
obscures  the  first  sound.  The  site  of  maximum  intensity  of  the 
murmur  is  usually  about  the  junction  of  the  fifth  and  sixth  left 
costal  cartilages  with  the  sternum,  or  over  the  ensiform  cartilage. 


2i6  DISEASES    OF   THE    HEART 

The  bruit  is  propagated  upwards  and  to  the  right,  and  outwards 
it  may  be  heard  as  far  as  the  apex. 

The  absence  of  the  murmur  does  not  exclude  the  existence  of 
tricuspid  incompetence. 

The  pulmonary  second  sound  is  weak,  or  diminished  in  intensity 
if  previously  accentuated. 

Reduplication  of  the  second  sound  at  the  base  is  also  commonly 
observed. 

DIAGNOSIS 

A  systolic  murmur  audible  in  the  tricuspid  area  may  be  the  sole 
evidence  of  slight  leakage  through  the  right  auriculo-ventricular 
opening.  The  precise  significance  of  such  a  murmur  would  be 
determined  by  attention  to  its  site  of  maximum  intensity,  and 
direction  of  transmission. 

If  the  signs  of  enlargement  of  the  right  heart  and  of  the  liver  are 
observed  in  association  with  a  systolic  murmur  in  the  tricuspid  area, 
the  presence  of  tricuspid  incompetence  is  hardly  open  to  doubt.  The 
diagnosis  would  be  confirmed  by  venous  pulsation  in  the  neck,  or 
by  pulsation  of  the  liver.  Moreover,  the  diagnostic  significance 
of  these  two  signs  is  not  weakened  by  the  absence  of  the  systolic 
murmur.  In  endeavouring  to  ascertain  whether  tricuspid  incom- 
petence is  primary,  or  secondary,  it  is  necessary  to  take  into  con- 
sideration the  circumstances  under  which  the  lesion  has  arisen,  as 
well  as  the  condition  of  the  left  heart  and  pulmonic  circulation. 


THE  ESTIMATION  OF  THE  AMOUNT  OF  REGURGITATION 
IN  TRICUSPID  INCOMPETENCE 

In  attempting  to  estimate  the  amount  of  regurgitation  in  tricuspid 
incompetence  the  observer  must  be  guided  by  the  general  principles 
laid  down  in  the  foregoing  chapters. 

The  precise  estimation  of  the  amount  of  leakage  is  of  less  im- 
portance than  the  determination  of  the  exact  causes  which  have  led 
to  the  occurrence  of  the  lesion. 

Thus  tricuspid  regurgitation,  secondary  to  disease  of  the  lungs 
or  left  heart,  is  always  an  event  of  serious  significance,  yet  the 
gravity  of  the  outlook  is  but  sHghtly  affected  by  the  degree  of 
insufficiency  which  obtains. 

Briefly,  the  chief  points  to  be  considered  in  the  estimation  of  the 
amount  of  regurgitation  in  tricuspid  incompetence  are  : — 

1.  The  degree  of  enlargement  of  the  right  auricle  and  ventricle. 

2.  The  presence  or  absence  of  venous  pulsation  in  the  neck. 

3.  The  presence  or  absence  of  pulsation  of  the  liver  and  the 

degree  of  enlargement  of  the  organ. 

4.  The  degree  of  arterial  anaemia. 


CHAPTER  XVI 
TRICUSPID    STENOSIS 


Pathogenesis— Morbid  Anatomy — Effects  on  the  Heart  and  Circulation — Symp- 
toms— Physical  Signs — Diagnosis — Estimation  of  degree  of  Stenosis. 

^ETIOLOGICAL  PATHOLOGY 

Tricuspid  stenosis  occurs  in  rare  instances  as  a  congenital  mal- 
formation, when  it  is  almost  invariably  associated  with  other 
developmental  anomalies  of  the  heart,  as,  for  instance,  patency  of 
the  foramen  ovale,  incomplete  ventricular  septum,  stenosis  of  the 
pulmonary  artery,  etc. 

The  acquired  form  of  the  disease  is  more  common  in  women 
than  men,  and  is  usually  secondary  to  and  probably  dependent  on 
stenosis  at  the  mitral  orifice  for  the  following  reasons: — 

1.  The  almost  constant  association  of  the  two  lesions  in  adults. 

2.  Both  lesions  occur  more  commonly  in  women  than  men,  the 

ratio  in  each  case  being  about  the  same,  i.e.  as  three  or  four 
to  one.  No  such  disproportion  exists  between  the  sexes 
in  the  liability  of  the  heart  to  right-sided  endocarditis  apart 
from  this  association  of  mitral  and  tricuspid  stenosis.  The 
inference  is,  therefore,  that  the  relationship  between  the  two 
lesions  is  causal. 

3.  The  remarkable  fact  that  the  degree  of  narrowing  at  the  mitral 

opening  is  always  greater  than  that  at  the  tricuspid  orifice. 

If  it  be  admitted  that  the  two  lesions  are  related  in  the  manner 
suggested,  the  occurrence  of  tricuspid  stenosis  is  explained  by  the 
long-continued  strain  and  irritation  to  which  the  valve  is  exposed 
in  consequence  of  the  rise  of  pressure  in  the  right  ventricle  follow- 
ing the  obstruction  at  the  mitral  orifice.  This  irritation  might  lead 
to  chronic  thickening,  whether  inflammatory  or  otherwise,  of  the 
structures  forming  the  tricuspid  orifice  and  valve,  which  under 
suitable  conditions  would  terminate  in  stenosis  of  the  tricuspid 
orifice. 

The  degree  of  narrowing  at  the  tricuspid  opening  is  less  than 

217 


2i8  DISEASES    OF   THE    HEART 

that  at  the  mitral  orifice,  because  of  its  later  onset  and  consequently 
shorter  duration. 

Tricuspid  stenosis  is  sometimes,  though  rarely,  observed  as  a 
solitary  lesion,  and  in  such  cases  it  is  reasonable  to  suppose  that 
the  affection  is  the  sequel  of  a  right-sided  endocarditis,  which,  as 
Byrom  Bramwell  has  urged,  is  probably  more  common  than  is 
generally  supposed.  The  morbid  changes  which  give  rise  to  narrow- 
ing of  the  tricuspid  orifice  are  similar,  for  the  most  part,  to  those 
observed  in  obstruction  at  the  mitral  opening. 

PATHOLOGICAL   RESULTS 

Effects  on  the  heart  and  circulation. — The  interference  with  the 
flow  of  blood  through  the  tricuspid  orifice  increases  the  work  of 
the  right  auricle,  and  thereby  gives  rise  to  hypertrophy  of  its  walls. 
A  certain  amount  of  dilatation  of  the  chamber  also  takes  place, 
probably  because  the  degree  of  hypertrophy  is  insufficient  to  enable 
the  auricle  to  completely  empty  itself. 

Moreover,  stenosis  of  the  tricuspid  opening  is  usually  accom- 
panied by  more  or  less  incompetence  of  the  valve,  so  that  dilatation 
of  the  auricle  may,  in  part  at  least,  be  due  to  overfilling. 

The  enlargement  of  the  right  auricle  in  tricuspid  stenosis  is 
commonly  very  remarkable. 

Engorgement  of  the  portal  and  systemic  venous  circulations  is 
an  early  and  prominent  feature  of  the  disease,  and  is  produced  in 
the  manner  described  in  previous  chapters. 

The  diminished  supply  of  blood  to  the  lungs,  left  heart,  and 
aorta  leads  to  a  greater  or  less  degree  of  arterial  anaemia.  The 
hypertrophy  and  dilatation  of  the  right  ventricle  which  is  usually 
observed  is  due  to  the  concurrent  narrowing  of  the  mitral  opening. 
The  presence  of  pulmonic  congestion  depends  upon  the  same  cause. 

SYMPTOMS 

The  symptoms  resemble  those  of  mitral  disease,  complicated  by 
tricuspid  incompetence.  Infra-mammary  or  epigastric  pain  is  fre- 
quently a  very  pronounced  symptom,  and  it  may  be  associated 
with  palpitation  and  great  dyspnoea. 

PHYSICAL  SIGNS 

Physiognomy. — Cyanosis  of  the  face,  lips,  and  ears  is  commonly 
observed,  and  the  extremities  are  usually  cold,  livid,  and  more  or 
less  oedematous. 

Dropsy  is  present  in  a  variable  degree  in  every  case,  and  it  may 
amount  to  complete  waterlogging  of  the  patient.  In  this  respect 
tricuspid  stenosis  offers  a  marked  contrast  to  mitral  obstruction, 


TRICUSPID   STENOSIS  219 

which  per  se  seldom  gives  rise  to  much  dropsy.  Indeed,  so  rarely 
is  this  the  case  that,  as  Sir  William  Broadbent  has  pointed  out, 
the  occurrence  of  severe  dropsy  in  the  course  of  uncomplicated 
mitral  stenosis  justifies  a  diagnosis  of  concurrent  obstruction  at  the 
tricuspid  opening. 

Pulse. — The  pulse  of  tricuspid  obstruction  presents  the  characters 
described  under  mitral  stenosis. 

Heart. — The  jugular  veins  are  distended  and  turgid,  and  the 
liver  is  enlarged,  but  pulsation  is  not,  as  a  rule,  observed  in  either 
situation.  If,  as  sometimes  happens,  jugular  pulsation  can  be 
detected,  it  is  due  to  the  refluent  current  that  is  produced  by  the 
auricular  systole. 

Epigastric  pulsation  is  usually  well  marked,  and  the  impulse  of 
the  right  ventricle  is  forcible  until  failure  of  the  heart  supervenes. 

A  presystolic  thrill  can  sometimes  be  detected  in  the  tricuspid 
area. 

The  area  of  cardiac  dulness  is  increased  laterally,  and  may  extend 
from  an  inch  to  an  inch  and  a  half  outside  the  right  sternal  edge. 

The  dulness  is  most  marked  in  the  third,  fourth,  and  fifth  right 
intercostal  spaces. 

A  presystolic  or  diastolic  bruit  may  be  heard  in  the  tricuspid  area, 
and  it  is  usually  accompanied  by  a  soft  blowing  systolic  murmur, 
which  follows  and  does  not  obscure  the  first  sound.  The  presystolic 
bruit  is  exceedingly  inconstant,  and  may  be  easily  overlooked  unless 
repeated  and  careful  auscultation  of  the  tricuspid  area  be  carried 
out. 

The  sounds  at  the  base  of  the  heart  are  usually  weak. 


DIAGNOSIS 

If  the  signs  of  enlargement  of  the  right  heart  are  observed  in 
conjunction  with  a  presystolic  or  diastolic  bruit,  which  is  limited 
to  the  tricuspid  area,  a  diagnosis  of  tricuspid  stenosis  can  be  made 
without  hesitation. 

As  a  rule,  however,  it  is  extremely  difficult,  and  often  impossible, 
to  decide  that  the  murmur  heard  in  the  tricuspid  area  is  not  due 
to  the  conduction  of  the  concurrent  presystolic  bruit  from  the  mitral 
region.  It  is  therefore  necessary  to  search  for  other  evidence  of 
tricuspid  obstruction. 

If  mitral  regurgitation  can  be  excluded,  the  occurrence  of  serious 
dropsy  in  the  course  of  mitral  stenosis  would  point  to  the  presence 
of  tricuspid  obstruction. 

Another  feature  of  considerable  significance  is  the  effect  of  the 
systolic  murmur,  which  is  usually  heard  in  the  tricuspid  area  on 
the  first  sound.  If  the  murmur  foUoivs  and  does  not  obscure  the 
first  sound,  the  amount  of  regurgitation  through  the  tricuspid  orifice 


220  DISEASES    OF   THE    HEART 

cannot  be  great.  If,  at  the  same  time,  the  signs  of  portal  and 
systemic  venous  engorgement  and  of  enlargement  of  the  right  side 
of  the  heart  are  more  pronounced  than  the  degree  of  insufficiency 
would  account  for,  the  presence  of  tricuspid  stenosis  may  reasonably 
be  suspected. 

Again,  since  regurgitation  through  the  tricuspid  orifice  tends  to 
destroy  the  first  sound,  while  stenosis  tends  to  shorten  and  exag- 
gerate it,  the  presence  of  a  sharp  and  loud  first  sound,  accompanied 
by  a  systolic  murmur,  would  be  evidence  in  favour  of  the  presence 
of  stenosis. 

Mackenzie  considers  that  presystolic  {i.e.  auricular  systolic) 
pulsation  of  the  liver  suggests  the  presence  of  tricuspid  stenosis. 
The  phenomenon  depends,  of  course,  on  the  backflow  of  blood 
into  the  hepatic  veins  that  may  be  produced  by  the  auricular 
contraction. 

ESTIMATION  OF  THE  DEGREE  OF  NARROWING 
IN  TRICUSPID  STENOSIS 

Since  compensation  to  any  effective  degree  is  impossible,  the 
estimation  of  the  amount  of  stenosis  has  a  purely  scientific  interest 

The  chief  sources  of  information  are — 

1.  The  degree  of  enlargement  of  the  right  auricle 

2.  The  extent  of  the  systemic  and  portal  congestion 

3.  The  degree  of  arterial  ansemia 


CHAPTER   XVII 
PULMONARY    INCOMPETENCE 


Pathogenesis — Morbid  Anatomy — Effects  on  the  Heart  and  Circulation — Associa- 
tion with  other  Cardiac  Developmental  Anomalies — Symptoms — Physical 
Signs — Diagnosis — Estimation  of  the  amount  of  Regurgitation. 

iETIOLOGICAL  PATHOLOGY 

Incompetence  of  the  pulmonic  valve  is  an  exceedingly  rare  con- 
dition. It  occasionally  occurs  as  a  congenital  malformation,  when  it 
is  nearly  always  combined  with  constriction  of  the  orifice. 

According  to  Barie,  pulmonic  insufficiency,  as  an  acquired  lesion, 
is  found  most  frequently  between  the  ages  of  eighteen  and  thirty- 
four.  The  endocardial  inflammation,  on  which  the  valvular  incom- 
petence depends,  usually  arises  in  connection  with  rheumatism,  or 
with  one  of  the  acute  infectious  fevers. 

In  rare  instances  pulmonic  regurgitation  is  the  result  of  malignant 
endocarditis. 

Degenerative  processes,  in  the  form  of  sclerosis  or  atheroma  of 
the  valve,  are  very  uncommon,  but  they  have  occasionally  been 
described  in  connection  with  both  the  congenital  and  acquired 
varieties  of  pulmonic  incompetence. 

There  can  be  no  doubt  that  relative  incompetence  of  the  pulmonic 
valve  does  sometimes  occur,  but  the  lesion  is  decidedly  rare.  It 
depends  on  the  stretching  of  the  pulmonic  orifice  that  may  be 
produced  by  high  pressure  in  the  pulmonary  artery,  such  as,  for 
instance,  may  obtain  in  cases  of  mitral  stenosis. 

Pulmonic  incompetence  due  to  congenital  malformation  of  the 
valve,  depends,  as  already  explained,  on  alterations  in  the  number, 
shape,  or  size  of  the  cusps,  which  are  consequently  unable  to 
efficiently  close  the  orifice. 

The  morbid  changes,  in  the  acquired  form  of  the  disease,  lead  to 
thickening,  induration,  and  distortion  of  the  cusps,  so  that  they  are 
unable  to  come  into  complete  apposition.  In  occasional  instances 
ulceration  or  perforation  of  the  cusps  is  the  cause  of  the  valvular 
insufficiency. 


222  DISEASES   OF  THE    HEART 

Incompetence  of  the  pulmonic  valve  is  frequently  combined  with 
constriction  of  its  orifice. 


PATHOLOGICAL   RESULTS 
Effects  on  the  Heart  and  Circulation 

The  right  ventricle,  which  is  now  supplied  with  blood  from  two 
sources,  undergoes  dilatation  from  overfilling.  It  subsequently 
hypertrophies  in  consequence  of  the  additional  work  entailed  in  the 
propulsion  of  a  greater  quantity  of  blood  than  normal. 

It  is  by  means  of  dilatation  and  hypertrophy  of  the  right  ventricle 
that  compensation  is  established  in  pulmonic  incompetence. 

Sooner  or  later  relative  incompetence  of  the  tricuspid  valve 
becomes  estabhshe^,  and  this  is  followed  by  dilatation  and  hyper- 
trophy of  the  right  auricle,  and  by  engorgement  of  the  portal  and 
systemic  veins  in  the  manner  previously  described. 

The  diminished  supply  of  blood  to  the  lungs  and  left  heart  leads 
to  a  greater  or  less  degree  of  arterial  ansemia. 

In  congenital  cases  pulmonary  incompetence  is  often  found  to  be 
associated  with  other  developmental  anomalies,  as,  for  instance, 
patency  of  the  ductus  arteriosus,  or  of  the  foramen  ovale,  or  im- 
perfect ventricular  septum. 


SYMPTOMS 

So  long  as  compensation  is  good,  the  symptoms  are  mainly  those 
of  derangement  of  the  pulmonic  circulation.  Thus  the  patient 
usually  suffers  from  cough  and  shortness  of  breath,  especially  on 
exertion,  and  these  symptoms  are  intensified  by  the  pulmonary 
complications,  such  as  bronchitis,  emphysema,  or  tuberculosis  of 
the  lungs,  which  frequently  coexists  with  the  valvular  affection. 

After  the  establishment  of  tricuspid  regurgitation,  the  signs  and 
symptoms  of  general  venous  stasis  make  their  appearance.  Death 
is  usually  due  to  gradual  failure  of  the  right  heart. 

In  pulmonic  incompetence  due  to  congenital  causes,  the  evidences 
of  portal  and  systemic  venous  embarrassment  are  present  to  a  greater 
or  less  degree  from  the  time  of  birth. 


PHYSICAL  SIGNS 

Physiognomy. — The  aspect  of  the  patient  is  frequently  suggestive 
of  imperfect  aeration  of  the  blood,  and  this  is  especially  noticeable 
in  cases  of  congenital  origin.  Clubbing  of  the  fingers  is  also 
commonly  found. 


PULMONARY   INCOMPETENCE  223 

The  signs  of  anaemia  are  sometimes  very  pronounced  in  the 
acquired  form  of  the  disease. 

The  occurrence  of  tricuspid  regurgitation  is  followed  by  dropsy, 
which  may  be  very  extensive. 

Pulse. — The  pulse  does  not,  as  a  rule,  present  any  features  of 
special  interest.     It  may  be  irregular,  both  in  force  and  frequency. 

The  radial  artery  is  usually  small  and  easily  compressible,  and  the 
pulse  wave  short,  weak,  and  badly  sustained. 

Heart. — If  the  tricuspid  valve  is  incompetent,  the  jugular  veins 
will  be  turgid  and  distended.     They  may  also  exhibit  pulsation. 

The  signs  of  enlargement  of  the  liver  will  likewise  be  observed. 

Pulsation  is  occasionally  seen  in  the  intercostal  spaces  to  the  right 
of  the  sternum.  Epigastric  pulsation  is  well  marked,  and  the  area 
of  cardiac  dulness  is  increased  chiefly  towards  the  right. 

It  is  sometimes  possible  to  detect  a  diastolic  thrill  in  the  pulmonic 
area. 

A  diastolic  murmur,  partially  or  wholly  replacing  the  second 
sound,  is  audible  to  the  left  of  the  sternum  over  the  base  of  the 
heart.  The  site  of  maximum  intensity  of  the  murmur  is  situated 
over  the  second  left  intercostal  space'  close  to  the  sternum,  or  over 
the  third  left  costal  cartilage. 

The  murmur,  which  may  be  soft  and  blowing,  or  rough  and  rasp- 
ing in  character,  is  propagated  downwards  and  to  the  right. 

The  pulmonic  second  sound  is  weak  or  inaudible. 


DIAGNOSIS 

The  chief  difficulty  in  the  diagnosis  of  pulmonic  regurgitation  is 
the  exclusion  of  aortic  insufficiency. 

The  differential  diagnosis  of  the  two  conditions  rests  on  the 
following  considerations. 

1.  Tlie  pulse. — The  characteristic  collapse  of  the  pulse  in  aortic 
insufficiency  is  not  present  in  the  pulmonic  lesion. 

2.  Tlie  cardiac  physical  signs. — Pulmonic  regurgitation  is  accom- 
panied by  the  signs  of  enlargement  of  the  right  ventricle,  whereas 
the  corresponding  aortic  lesion  is  attended  by  enlargement  of  the 
left  ventricle. 

The  absence  of  the  second  sound,  or  the  presence  of  a  diastolic 
bruit  over  the  carotid  arteries  in  the  neck,  would  be  evidence  in 
favour  of  aortic  insufficiency. 

The  presence  of  great  venous  engorgement,  with  jugular  or  hepatic 
pulsation,  would,  on  the  other  hand,  indicate  incompetence  of  the 
pulmonic  rather  than  of  the  aortic  valve. 


224  DISEASES    OF   THE    HEART 

Cyanosis  and  clubbing  of  the  fingers  would  bear  a  like  inter- 
pretation. 

If  the  two  lesions  are  combined  a  diiferential  diagnosis  may  be 
impossible. 

ESTIMATION   OF  THE  AMOUNT  OF  REGURGITATION 
IN   PULMONIC   INCOMPETENCE 

The  degree  of  insufficiency  is  determined  from  the  following  data : — 

1,  The  degree  of  enlargement  of  tlie  right  ventricle. — So  long 
as  compensation  is  satisfactory,  the  degree  of  enlargement  of  the 
right  ventricle  is  a  measure  of  the  amount  of  regurgitation. 

2.  The  presence  or  absence  of  the  pulmonic  second  sound. — If 

the  murmur  follows  and  does  not  obscure  the  second  sound,  the 
amount  of  regurgitation  is  probably  slight.  Complete  obliteration 
of  the  second  sound  is  an  indication  of  serious  incompetence  of 
the  valve. 


CHAPTER    XVIII 
PULMONARY    STENOSIS 


Pathogenesis— Morbid  Anatomy— Effects  on  the  Heart  and  Circulation— Symp- 
toms—Physical  Signs— Diagnosis— Estimation  of  the  degree  of  Stenosis. 

iETIOLOGICAL    PATHOLOGY 

With  very  rare  exceptions  the  origin  of  pulmonary  stenosis  dates 
from  foetal  life,  and  the  lesion  constitutes  one  of  the  commonest  as 
well  as  one  of  the  most  important  forms  of  congenital  disease  of  the 
heart. 

Three  varieties  of  narrowing  may  be  observed,  viz.  (i)  stenosis  of 
the  orifice,  (2)  atresia  of  the  orifice  and  first  part  of  the  artery, 
(3)  stenosis  of  the  conus  arteriosus. 

In  the  first  event  the  obstruction  is  due  to  intra-uterine  endo- 
carditis, which  leads  to  adhesion  of  the  cusps  and  contraction  of 
the  fibrous  ring  forming  the  orifice  of  the  vessel.  In  some  cases 
the  opening  is  partially  blocked  by  luxuriant  vegetations,  which  may 
be  formed  after  birth. 

Atresia  of  the  orifice  and  first  part  of  the  pulmonary  artery  is 
always  a  developmental  anomaly,  and  is  invariably  associated  with 
other  malformations  of  the  heart,  such  as  patency  of  the  ductus 
arteriosus  or  foramen  ovale,  imperfect  ventricular  septum,  etc. 

Stenosis  of  the  conus  arteriosus  may  be  due  to  errors  of  develop- 
ment, but  in  many  instances  it  is,  no  doubt,  the  result  of  myocarditis 
with  subsequent  sclerosis. 

Pulmonary  stenosis,  as  an  acquired  lesion,  is  attributable,  in  most 
instances,  to  endocarditis.  Rheumatism  and  the  acute  infectious 
fevers  have  been  the  exciting  cause  of  the  endocardial  inflammation 
in  some  cases.  In  others  the  lesion  has  appeared  to  depend  on 
chronic  inflammatory  or  atheromatous  changes,  the  result  of  long- 
continued  strain. 

Direct  violence  has  also  been  recorded  as  an  exciting  cause  of 
pulmonary  stenosis. 

The  formation  of  vegetations  in  the  course  of  malignant  endo- 
carditis occasionally  leads  to  obstruction  at  the  pulmonic  orifice. 
Q  225 


226  DISEASES   OF   THE   HEART 

PATHOLOGICAL   RESULTS 
Effects  on  the  Heart  and  Circulation 

In  congenital  cases  the  effect  on  the  heart  depends  largely  on  the 
stage  of  cardiac  development  at  which  the  pulmonary  narrowing  is 
produced.  If  it  appears  before  the  end  of  the  third  month,  the 
interventricular  septum  does  not  close  ;  if  after  this  date,  the  foramen 
ovale  and  ductus  arteriosus  may  remain  patent.  The  condition  of 
the  right  ventricle  varies  with  the  degree  of  occlusion  of  the  pulmonic 
orifice.  If  the  opening  is  completely  blocked  the  ventricle  mav 
remain  small  and  undeveloped,  but  with  less  degrees  of  narrowing 
the  chamber  is  commonly  greatly  hypertrophied. 

Since  incompetence  of  the  pulmonic  valve  is  usually  combined 
with  stenosis  of  the  opening,  the  ventricle  is  also  found  to  be  more 
or  less  dilated. 

The  cardiac  changes  associated  with  the  acquired  form  of  pul- 
monary obstruction  resemble,  for  the  most  part,  those  described  in 
connection  with  pulmonary  incompetence. 

The  establishment  of  tricuspid  regurgitation  is  followed  by  the 
usual  train  of  events,  culminating  in  portal  and  systemic  venous 
engorgement,  dropsy,  etc.  The  diminished  supply  of  blood  to  the 
lungs  leads  to  more  or  less  arterial  anaemia. 

The  subjects  of  both  the  congenital  and  acquired  forms  of  pul- 
monic obstruction  are  especially  liable  to  chronic  tuberculosis  of 
the  lungs,  which  in  a  large  proportion  of  the  cases  is  the  cause 
of  death. 

SYMPTOMS 

In  severe  cases  of  the  congenital  form  of  the  lesion  the  child  may 
not  survive  its  birth  by  more  than  a  few  hours  or  days. 

Cyanosis  is  usually  a  pronounced  feature,  and  is  accompanied  by 
dyspnoea  and  the  signs  of  general  venous  distension.  The  tempera- 
ture is  often  sub-normal,  and  the  fatal  termination  may  be  preceded 
by  drowsiness,  coma,  or  convulsions. 

In  less  severe  examples  of  congenital  pulmonic  stenosis  life  may 
be  prolonged  for  many  years,  but,  with  few  exceptions,  the  patient 
dies  before  the  age  of  puberty  from  chronic  pulmonary  tuberculosis. 

In  cases  of  this  kind  there  is  usually  more  or  less  lividity  of  the 
face  and  extremities,  especially  on  exertion,  and  the  superficial 
veins  appear  distended.  Clubbing  of  the  fingers  and  toes  is 
commonly  observed,  and  the  general  nutrition  and  growth  of  the 
body  is  often  seriously  interfered  with. 

Dropsy  does  not  appear  as  a  rule  until  compensation  fails,  but 
it  may  follow  urgent  cardiac  symptoms  consequent  on  intercurrent 
pulmonary  compHcations. 


PULMONARY   STENOSIS  227 

Shortness  of  breath  on  exertion,  cough,  palpitation  of  the  heart, 
etc.,  are  common  symptoms. 

The  superficial  temperature  is  commonly  reduced,  and  the  patient 
frequently  complains  of  chilliness  on  the  least  exposure. 

Pulmonary  complications,  such  as  bronchitis,  emphysema,  and 
tuberculosis  of  the  lungs,  are  often  observed,  and  the  latter  disease 
may  be  a  cause  of  haemoptysis. 

Interference  with  the  cerebral  circulation  may  give  rise  to  head- 
ache, giddiness,  drowsiness,  etc.,  and  there  may  be  impairment  of 
the  mental  powers. 

In  the  acquired  form  of  pulmonic  stenosis  there  may  be  no  symp- 
toms during  the  stage  of  compensation  beyond  slight  dyspnoea  on 
exertion.     Clubbing  of  the  fingers  is  usually  present. 

Failure  of  the  right  ventricle  and  the  consequent  production  of 
tricuspid  incompetence  is  followed  by  the  usual  signs  and  symptoms 
of  portal  and  systemic  venous  congestion. 

PHYSICAL    SIGNS 

Pulse. — The  pulse  of  pulmonic  stenosis  is  usually  small,  weak, 
and  irregulai\ 

Heart. — After  failure  of  the  right  ventricle  the  juguiar  vems  may 
appear  distended,  and  in  some  instances  they  exhibit  pulsation. 
An  increase  in  the  size  of  the  liver  is  also  observed. 

Inspection  may  show  bulging  of  the  prsecordiurh  in  the  lower 
sternal  region. 

Epigastric  pulsation  is  usually  well  marked,  and  is  associated  with 
a  strong  heaving  impulse. 

A  thrill,  systolic  in  time,  may  be  felt  in  the  pulmonic  area. 

The  area  of  cardiac  dulness  is  increased  towards  the  right,  corre- 
sponding with  the  enlargement  of  the  right  ventricle. 

A  systolic  murmur,  which  is  propagated  upwards  and  to  the  left, 
is  heard  in  the  pulmonic  area.  The  site  of  maximum  intensity  is 
situated  close  to  the  left  edge  of  the  sternum,  in  the  second  inter- 
space, or  at  the  level  of  the  third  costal  cartilage.  The  murmur 
is  not  heard  over  the  carotid  arteries,  but  in  congenital  cases  it 
may  be  audible  over  the  whole  prsecordium. 

The  character  of  the  bruit  varies  considerably.  In  some  instances 
it  is  harsh  and  loud,  in  others  soft  and  blowing. 

The  pulmonic  second  sound  is  weak,  and  may  be  accompanied 
by  a  diastolic  murmur. 

DIAGNOSIS 

The  site  of  maximum  intensity,  and  more  especially  the  direction 
of  propagation  of  the  murmur,  taken  in  conjunction  with  the  cardiac 
physical  signs  and  the  state  of  the  arterial  and  venous  circulations, 
would  be  sufficient  to  distinguish  pulmonary  obstruction  from  other 
valvular  lesions  of  the  heart.     The  exclusion  of  pleuro-pericardial 


228  DISEASES   OF   THE    HEART 

conditions  and  anaemia  as  the  possible  causes  of  a  systolic  murmur, 
audible  in  the  pulmonic  area,  would  rest  on  a  careful  consideration 
of  the  associated  symptoms  and  physical  signs. 

The  differential  diagnosis  of  pulmonary  stenosis  and  other 
congenital  affections  of  the  heart,  such  as  patent  ductus  arteriosus, 
imperfect  ventricular  septum,  etc.,  cannot  always  be  made  with 
certainty.  In  this  respect  more  significance  attaches  to  the  con- 
dition of  the  right  and  left  ventricles  than  to  the  site  of  maximum 
intensity  and  area  of  distribution  of  the  murmur.  Peacock  states 
that  if  a  case  of  congenital  disease  of  the  heart  survive  the  twelfth 
year,  the  probabilities  are  greatly  in  favour  of  the  existence  of 
pulmonary  stenosis.  The  differentiation  between  the  congenital 
and  acquired  forms  of  pulmonary  stenosis  rests  almost  entirely  on 
the  history  of  the  case. 

ESTIMATION  OF  THE  DEGREE  OF  NARROWING  IN 
PULMONARY  STENOSIS 

The  data  which  supply  most  information  on  this  point  are : — 

1.  The  amount  of  hypertrophy  of  the  right  ventricle 

2.  The  degree  of  arterial  anaemia 


CHAPTER   XIX 
COMBINED   VALVULAR    DISEASE 

The  common  combination  of  aortic  stenosis  and  incompetence 
and  of  mitral  stenosis  and  incompetence  has  already  been  pointed 
out.  A  like  combination  of  lesions  is  also  observed  at  the  pul- 
monic and  tricuspid  openings. 

Reference  has  iiicewise  been  made  to  the  frequent  association  of 
mitral  with  aortic  disease  and  of  tricuspid  with  mitral  affections. 

Thus  mitral  stenosis  may  occur  in  combination  with  aortic  stenosis 
or  aortic  regurgitation  or  with  both  these  lesions.  Again  mitral 
incompetence  may  be  combined  with  one  or  both  forms  of  aortic 
disease,  or  combined  mitral  disease  may  be  found  in  association 
with  either  or  both  aortic  lesions.  The  frequent  association  of 
valvular  defects  on  the  right  and  left  sides  of  the  heart  has  already 
been  mentioned,  and  the  significance  of  the  various  combinations 
that  may  occur  has, also  been  considered. 

The  method  of  production  of  the  different  combinations  may  be 
inferred  from  what  has  been  said  on  the  subject  of  chronic  valvular 
disease  of  the  heart. 

In  all  forms  of  combined  valvular  affections,  however  complex, 
each  lesion  is  represented  by  its  own  particular  physical  signs. 

With  respect  to  the  diagnosis  of  combined  valvular  disease,  as 
much  importance  attaches  to  the  secondary  effects  of  each  lesion 
on  the  heart  and  circulation  as  to  the  presence  of  distinctive 
auscultatory  phenomena. 

For  instance,  the  presence  of  true  jugular  or  hepatic  pulsation  in 
the  course  of  mitral  disease  would  justify  a  diagnosis  of  a  con- 
comitant tricuspid  regurgitation,  even  in  the  absence  of  auscultatory 
evidence  of  the  latter  lesion. 

The  estimation  of  the  severity  of  the  various  lesions  comprising 
any  combination  is  based  on  the  considerations  which  were  enumer- 
ated in  connection  with  the  diseases  of  the  individual  valves. 


229 


CHAPTER   XX 

PROGNOSIS    OF   CHRONIC   VALVULAR 
DISEASE 


Site  and  Form  of  Lesion — Mode  of  Origin  and  Extent  of  Lesion — Condition  of 
Cardiac  ]\Iuscle — State  of  Peripheral  Vessels — General  Health  of  Patient,  etc. 
— Presence  or  Absence  of  Complications. 

The  considerations  upon  which  the  prognosis  of  chronic  valvular 
disease  of  the  heart  is  based  may  be  conveniently  arranged  and 
discussed  under  the  following  heads  : — 

The  Site  and  Form  of  the  Lesion 

The  gravity  of  chronic  valvular  disease  is  determined  to  some 
extent  by  the  seat  and  form  of  the  affection,  though  this  element 
in  the  prognosis  is  liable  to  so  many  exceptions  that  it  does  not 
carry  great  weight.  Moreover,  observers  are  not  yet  agreed  as  to 
the  relative  danger  attending  different  varieties  of  valvular  disease. 

Provided  compensation  is  efficient,  the  prognosis,  at  all  events 
before  middle  age,  is  more  favourable  in  aortic  than  in  mitral 
lesions.  On  the  other  hand,  if  the  heart  fails,  the  prospect  of 
recovery  is  better  in  mitral  disease  than  in  aortic.  Speaking 
generally,  the  prognosis  is  more  favourable  in  aortic  stenosis  than 
in  aortic  regurgitation,  and  in  mitral  regurgitation  than  in  mitral 
stenosis.  The  relative  gravity  of  left-sided  valvular  lesions  of  the 
heart  is  probably  fairly  accurately  represented  by  the  following 
order,  beginning  with  the  most  serious  affection,  viz.  (i)  aortic 
regurgitation ;  (2)  mitral  stenosis ;  (3)  aortic  stenosis ;  (4)  mitral 
regurgitation.  Of  right-sided  lesions,  pulmonary  stenosis  affords 
the  most  hopeful  prognosis. 

"  Tricuspid  regurgitation,  secondary  to  disease  on  the  left  side 
of  the  heart,  is  probably  more  serious  than  any  other  form  of 
chronic  valvular  affection. 

Aortic  insufficiency  is  the  only  form  of  valvular  disease  that  is 
liable  to  give  rise  to  sudden  death. 

230 


CHRONIC  VALVULAR  DISEASE  231 


The  Mode  of  Origin  of  the  Lesion 

Valvular  rupture,  which  is,  however,  very  rare,  constitutes  the 
most  dangerous  form  of  origin,  and  may  be  rapidly  fatal.  An  acute 
valvulitis  is  less  serious  than  chronic  inflammation  or  atheromatous 
disease  of  the  valves,  since  the  effects  in  the  first  event  are  usually 
stationary,  while  in  the  second  they  are  progressive.  Furthermore 
the  conditions  under  which  chronic  inflammation  or  atheromatous 
disease  of  the  valves  occur  militate  greatly  against  the  establishment 
of  adequate  compensation. 

As  a  rule  the  effects  of  an  acute  valvulitis  are  permanent  and 
stationary,  but  an  exception  to  this  statement  must  be  noted  in  the 
case  of  mitral  stenosis,  in  which  the  narrowing  tends  to  become  more 
pronounced  in  consequence  of  the  contraction  of  the  newly-formed 
fibrous  tissue.  It  is  this  circumstance  which  adds  to  the  gravity  of 
the  prognosis  in  cases  of  mitral  stenosis.  Progressive  narrowing  of 
the  opening  may  also  occur  in  aortic  stenosis,  but  the  effects  of  the 
obstruction  in  this  event  are  more  easily  neutralised  than  in  the  case 
of  mitral  constriction. 

The  Extent  of  the  Lesion 

The  estimation  of  the  degree  of  obstruction  or  amount  of 
regurgitation,  as  the  case  may  be,  has  already  been  fully  considered 
under  the  account  of  the  diseases  of  the  different  valves.  The 
extent  of  the  lesion,  although  an  important  guide  to  the  severity 
of  the  case,  is  a  measure  of  the  gravity  of  the  outlook  only  when 
interpreted  in  the  light  of  the  other  prognostic  indications. 

The  Condition  of  the  Cardiac  Muscle 

The  state  of  the  myocardium,  which  forms  the  chief  element  in 
the  prognosis  of  chronic  valvular  disease,  is  largely  computed  from 
the  evidence  afforded  by  the  absence  or  presence  of  symptoms,  by 
the  physical  examination  of  the  heart  and  circulation,  and  by  the 
effects  of  treatment. 

An  absence  of  the  symptoms  and  signs  of  circulatory  disturbance 
argues  a  healthy  condition  of  the  myocardium,  and  justifies  a 
hopeful  prognosis.  Manifestations  of  cardiac  inadequacy  may 
appear  on  the  arterial  or  on  the  venous  side  of  the  circulation, 
in  consequence  of  the  imperfect  propulsion,  or  of  the  damming 
back  of  blood.  The  relative  proportions  of  hypertrophy  and  dilata- 
tion, and  the  strength  and  size  of  the  pulse  would  afford  further 
evidence  of  the  condition  of  the  cardiac  muscle. 

A  history  of  repeated  attacks  of  rupture  of  compensation,  or  of 
gradual  failure  of  the  heart  without  adequate  cause,  is  of  grave 
import.     Long-continued  visceral  congestion,  accompanied  by  severe 


232  DISEASES    OF   THE    HEART 

dyspnoea,  dyspepsia,  albuminuria,  or  dropsy  of  the  extremities  and 
serous  cavities,  renders  the  outlook  very  grave. 

The  absence  of  any  response  to  treatment  implies  exhaustion  of 
the  cardiac  muscle  and  warrants  a  most  unfavourable  prognosis. 

The  State  of  the  Peripheral  Vessels 

Arterial  degeneration  is  serious  on  account  of  the  increased  strain 
thereby  thrown  on  the  heart.  Moreover,  rupture  of  the  diseased  wall 
may  be  followed  by  fatal  haemorrhage  into  the  brain  or  elsewhere. 

Atheromatous  disease  of  the  coronary  arteries  may  directly  inter- 
fere with  the  nutrition  of  the  heart  by  impeding  the  circulation  of 
blood  through  the  organ. 

Habitual  high  arterial  tension  also  adds  to  the  danger  by  in- 
creasing the  work  of  the  cardiac  muscle. 

Petechias  are  of  bad  omen. 

The  General  Health  of  the  Patient 

The  state  of  general  nutrition,  the  presence  or  absence  of  ansemia, 
and  the  condition  of  the  assimilative  and  excretory  organs  are  the 
points  which  require  special  attention. 

The  absence  of  anaemia,  and  the  existence  of  a  good  standard 
of  general  health  are  favourable  signs. 

Persistent  congestion  of  the  organs  of  assimilation  and  excretion 
is  followed  by  more  or  less  deterioration  in  the  quality  of  the  blood 
which  seriously  interferes  with  the  nutrition  of  the  heart  and  other 
viscera,  and  in  this  way  materially  adds  to  the  gravity  of  the 
outlook. 

The  Age,  Sex,  Mode  of  Life,  and  Habits  of  the  Patient 

The  prognosis  of  chronic  valvular  disease  is  less  favourable  in 
childhood  than  during  adult  life,  on  account  of  the  liability  to  acute 
intercurrent  disease,  and  of  the  additional  strain  to  which  the  heart  is 
exposed  at  the  time  of  puberty,  more  especially  in  the  case  of  girls. 
Furthermore,  the  special  liability  of  the  female  sex  to  mitral  stenosis 
and  to  anasmia,  renders  the  outlook  more  serious  in  girls  than  in  boys. 

Again,  compensation  in  cases  of  valvular  disease  occurring  after 
the  age  of  forty  is  hardly  ever  satisfactory,  and  this  fact,  taken  in 
conjunction  with  the  tendency  to  arterial  and  myocardial  degenera- 
tion after  this  period  of  life,  is  of  considerable  importance  in  the 
estimation  of  the  probable  course  and  duration  of  the  lesion. 

Exposure,  insufficient  food,  laborious  occupations,  etc.,  add  greatly 
to  the  gravity  of  valvular  disease,  consequently  the  prognosis  is  much 
less  favourable  among  the  poorer  classes  than  among  the  well-to-do. 

Mental  strain  and  excitement,  and  over-indulgence  in  the  use  of 


CHRONIC    VALVULAR     DISEASE  233 

alcohol,  tea,  coffee,  food  of  all  kinds,  and  tobacco,  exercise  a  pre- 
judicial effect  on  the  course  of  the  disease. 

Temperament  appears  to  have  a  considerable  influence  for  good 
or  evil ;  at  all  events,  an  even,  happy  disposition  exerts  a  most  bene- 
ficial effect  on  the  production  and  maintenance  of  compensation.     — - 

Hereditary  tendencies  carry  very  great  weight  in  the  estimation  of 
the  probable  duration  of  life  in  cases  of  chronic  valvular  disease, 
inasmuch  as  the  liability  to  the  premature  development  of  arterial 
and  myocardial  degeneration  is  prone  to  run  in  families. 

The  Presence  or  Absence  of  Complications 

The  presence  of  complications,  more  especially  affections  of  the 
lungs  and  of  the  organs  which  subserve  assimilation  and  excretion, 
add  greatly  to  the  gravity  of  the  prognosis.  Even  in  the  absence 
of  complications,  an  accident  such  as  cerebral  embolism  may  lead 
quickly  to  a  fatal  termination,  and  thus  upset  an  otherwise  favourable 
prognosis.  Except,  however,  in  cases  of  aortic  regurgitation,  chronic 
valvular  disease  of  the  heart  seldom  gives  rise  to  sudden  death. 

It  goes  without  saying  that  the  gravity  of  valvular  disease  is 
increased  by  the  presence  of  pericardial,  myocardial,  or  endocardial 
complications. 

Pericardial  adhesion,  if  extensive,  exercises  a  particularly  baneful 
influence  on  the  establishment  and  maintenance  of  compensation. 

Recurrent  attacks  of  rheumatism  add  materially  to  the  gravity 
of  the  outlook  in  cases  of  chronic  valvular  disease. 


CHAPTER  XXI 

THE  TREATMENT   OF   CHRONIC 
VALVULAR   DISEASE 


Prophylaxis  —  Treatment  before  Failure  of  Compensation  —  Treatment  after 
Failure  of  Compensation — Removal  of  Cause — Treatment  of  Effects — Use 
of  Cardiac  Stimulants  and  Tonics. 

The  prophylactic  treatment  of  chronic  valvular  lesions  of  the  heart 
hardly  calls  for  comment,  since  the  incidence  of  endocardial  disease, 
whether  of  rheumatic  or  degenerative  origin,  cannot  be  prevented  by 
any  means  with  which  we  are  at  present  acquainted. 

At  the  same  time  much  may  be  done  to  delay  the  appearance 
and  retard  the  progress  of  chronic  valvular  changes,  more  especially 
when  these  are  dependent  on  cardiac  and  vascular  overstrain,  such 
as  obtains  in  case?  of  long- continued  high  arterial  tension,  or 
prolonged  muscular  exertion.  It  is  possible,  too,  that  the  influence 
of  gout,  syphiHs,  and  chronic  alcoholism,  etc.,  in  the  production  of 
atheromatous  disease  of  the  heart  and  vessels  may  to  some  extent  be 
controlled  by  treatment. 

In  practice,  however,  since  valvular  affections  of  the  heart,  with 
very  few  exceptions,  are  neither  preventable  nor  curable,  the  main 
objects  of  treatment  are,  on  the  one  hand,  to  promote  and  maintain 
changes  of  a  compensatory  nature,  and,  on  the  other,  to  ward  off, 
retard,  and  minimize  the  effects  of  the  lesion,  in  so  far  as  they  act 
injuriously  on  the  heart  and  circulation. 

In  considering  this  part  of  the  subject,  the  periods  before  and 
after  failure  of  compensation  will  for  convenience  of  description  be 
taken  separately. 


Treatment  before  Failure  of  Compensation 

From  a  clinical  point  of  view  the  essential  conditions  for  the 
production  of  compensation  in  cases  of  valvular  disease  following 
acute  endocarditis  are  time  and  rest.  The  period  that  must  elapse 
before  exercise  can  be  resumed  without  detriment  to  the  com- 
pensatory process  varies  by  weeks,  or  even  months,  and  depends, 

234 


CHRONIC   VALVULAR   DISEASE  235 

for  the  most  part,  on  the  site  and  extent  of  the  lesion.  Other 
things  being  equal,  the  time  required  for  the  establishment  of 
compensation  is  longer  in  the  case  of  aortic  than  of  mitral  disease, 
and  in  that  of  severe,  than  of  slight  affections. 

The  age  of  the  patient,  at  the  time  of  the  occurrence  of  the  lesion, 
also  exerts  a  most  important  influence  on  the  development  of  com- 
pensation, for  the  reason  that  hypertrophy  of  the  heart  originating 
after  forty  is  seldom  or  never  satisfactory.  When  it  happens  that 
the  endocardial  affection  is  chronic  from  the  beginning,  the  com- 
pensatory changes  frequently  keep  pace  with  the  progress  of  the 
valvular  defect. 

Again,  for  the  reasons  already  indicated  (see  p.  232),  compensation 
is  hardly  ever  satisfactory  in  those  cases  of  morbus  cordis  which 
become  established  before  the  age  of  puberty. 

In  any  event,  so  soon  as  compensation  has  been  affected,  the 
chief  aim  of  treatment  is  the  maintenance  of  the  nutrition  of  the 
cardiac  muscle. 

This  object  can  usually  be  satisfactorily  attained  by  the  intelligent 
observance  of  certain  hygienic  and  dietetic  rules,  the  operation  of 
which  may  be  supplemented,  when  necessary,  by  medicinal  means. 

Hygienic  Treatment. — The  patient  may  be  permitted  to  follow  his 
ordinary  occupation  and  habits,  provided  they  are  not  detrimental  to 
health,  and  do  not  impose  any  great  or  sudden  strain  on  the  heart. 

Exercise  in  the  fresh  air  is  essential,  and  should  be  encouraged  in 
every  way,  but  the  amount  that  may  be  indulged  in  with  safety  varies 
greatly  in  different  cases.  For  instance,  a  young  and  vigorous  adult 
may  take  part  with  benefit  in  the  less  arduous  outdoor  recreations, 
such  as  cricket,  tennis,  golf,  or  cycling,  etc.,  so  long  as  he  does  not 
experience  any  unusual  shortness  of  breath  or  palpitation  while  so 
engaged.  On  the  other  hand,  patients  of  middle  age,  and  more 
especially  those  of  sedentary  habits,  must  observe  much  greater 
caution  in  the  amount  of  exertion  that  they"  undertake. 

Exercise,  under  any  circumstances,  must  be  commenced  gradually, 
and  increased  slowly  and  judiciously  up  to  the  maximal  limit  consis- 
tent with  safety,  which  for  practical  purposes  is  defined  by  the  onset 
of  breathlessness,  palpitation,  a  feeling  of  fatigue  or  of  faintness. 

Sudden  or  violent  effort  ought  at  all  times  to  be  carefully  avoided. 

The  patient  will  derive  benefit  from  cheerful  surroundings,  and 
he  should  be  removed  so  far  as  practicable  from  all  sources  of 
mental  strain  and  excitement,  whether  pleasurable  or  otherwise. 

The  risk  of  exposure  to  cold,  damp,  and  sudden  changes  of  tem- 
perature may  be  lessened  by  the  adoption  of  woollen  or  flannel  under- 
clothing, which  should  be  worn  next  to  the  skin  all  the  year  round. 
Ordinary  common-sense  precautions  will  be  sufficient  to  guard  against 
the  danger  of  chill,  and  the  patient  should  be  impressed  with  the 
necessity  of  observing  a  reasonable  amount  of  care  in  this  respect. 

A  regular  daily  action  of  the  bowels  is  of  the  utmost  importance, 


236  DISEASES  OF  THE  HEART 

and  if  this  cannot  be  obtained  naturally,  it  must  be  procured  by 
medicinal  means.  A  tendency  to  constipation  may  be  met  by  a 
course  of  mild  saline  aperients,  which  is  usually  all  that  is  required. 

Many  cases  of  compensated  cardiac  disease  derive  great  benefit 
from  a  visit  to  the  seaside,  while  others  appear  to  do  better  at 
inland  places  situated  at  an  elevation  of  one  to  two  thousand  feet, 
where  the  climate  is  mild,  dry,  and  moderately  bracing. 

If  it  is  considered  advisable  to  communicate  to  the  patient  the 
nature  of  his  complaint,  the  information  should  be  conveyed  with 
the  utmost  caution  and  gentleness,  and  at  the  same  time  he  should 
be  encouraged  to  take  a  cheerful  and  sanguine  view  of  his  condition. 
The  fear  of  sudden  death,  which  in  the  large  majority  of  cases  is 
totally  groundless,  must  so  far  as  possible  be  allayed. 

Dietetic  treatment. — There  is  no  necessity  for  any  particular 
modification  of  the  diet  during  the  stage  of  compensation.  The 
patient  may  take  the  food  to  which  he  is  accustomed  so  long  as  it 
agrees  with  him  and  is  moderate  in  quantity. 

It  is  very  desirable,  however,  that  the  total  quantity  of  food  con- 
sumed in  the  twenty-four  hours  should  be  fairly  evenly  distributed 
over  the  three  principal  meals  of  the  day,  in  order  to  avoid  over- 
loading the  stomach  at  any  one  repast.  The  digestion  of  a  heavy 
meal  is  in  itself  a  source  of  considerable  circulatory  disturbance  and 
may,  by  this  means,  throw  an  injurious  amount  of  strain  on  the 
heart.  Furthermore,  the  ingestion  of  a  large  quantity  of  food  at  one 
time  must  give  rise  to  more  or  less  distension  of  the  stomach,  which, 
by  direct  pressure,  may  seriously  interfere  with  cardiac  action.  It 
is  in  this  way  that  flatulence  may  be  a  source  of  discomfort  or  even 
of  danger. 

Alcohol,  whether  in  the  form  of  wine,  beer,  or  spirits,  must  be 
taken  in  very  small  quantities  and  at  meal  times  only.  The 
existence  of  high  arterial  tension  is  an  indication  for  the  total 
prohibition  of  alcoholic  beverages,  as  well  as  for  considerable 
restriction  in  the  amount  of  nitrogenous  food. 

Tea  and  coffee  are  injurious  unless  taken  in  strict  moderation. 
Tobacco  must  be  used  sparingly,  on  account  of  its  depressing 
influence  on  the  heart  when   smoked  to  excess. 

Medicinal  treatment, — The  use  of  drugs  is  seldom  called  for  at 
this  period  of  the  disease,  since  the  general  health  of  the  patient  and 
the  nutrition  of  the  cardiac  muscle  are  usually  perfectly  well  main- 
tained by  the  measures  above  indicated. 

Nevertheless,  a  liability  to  the  appearance  of  anaemia  is  sometimes 
observed  even  under  the  most  favourable  hygienic  and  dietetic 
conditions,  and  it  then  becomes  necessary  to  give  haematinics,  such 
as  iron  and  arsenic,  with  which  may  be  combined  small  doses  of 
digitalis  or  strychnine. 

Iodide  of  potassium   with  arsenic  or  iron   make  a  very  suitable 


CHRONIC   VALVULAR   DISEASE  237 

combination  in   the   treatment  of  chronic   valvular   affections,  and 

these   drugs   are    more    particularly   indicated    in    those   cases    in 

which  syphilis  is  a  causal  factor.  ^^ 

The  following  are  illustrative  prescriptions  : —  ^^"^^ 

^     Tincturse  Ferri  Perchloridi  ...  nix. 

Liquoris  Strychninse  Hydrochloridi  niiii. 

Tincturse  Digitalis     ...         ...  ...  Tiiviii. 

Syrupi  Limonis         ...          ...  ...  5i- 

Glycerini        ...         ...         ...  ...  5i- 

Aquse               ...          ...     q.s.  ad  gi- 

Fiat  Mistura.  S.  Two  tablespoonfuls  to  be  taken  three  times  a  day 
after  meals. 

Or, 

!^     Ferri  et  Ammonii  Citratis    ...  ...  gr.x. 

Tincturse  Nucis  Vomicse      ...  ...  tilviii. 

Liquoris  Arsenicalis             ...  ...  ttiiii. 

Syrupi  Aurantii         ...         ...  ...  5ss. 

Aqu^  Chloroform!    ...      q.s.  ad  gi- 

Fiat  Mistura.  S.  Two  tablespoonfuls  to  be  taken  three  times  a  day 
after  food. 

Or, 

^     Ferri  et  Ammonii  Citratis  ...  ...  gr.x. 

Potassii  lodidi          ...  ...  ...  gr.iv. 

Liquoris  Arsenicalis  ...  ...  ttiiii. 

Spiritus  Chloroformi  ...  ...  trix.                      ■ 

Aquse  Menthse  Piperitse  q.s.  ad  §i. 

Fiat  Mistura.  S.  Two  tablespoonfuls  to  be  taken  three  times  a  day 
after  food. 

Medicinal  treatment  is,  however,  more  commonly  required  at  this 
stage  in  order  to  combat  the  effects  of  intercurrent  disease,  notably 
attacks  of  rheumatism  or  bronchial  catarrh,  which  may  seriously 
imperil  the  continuance  of  compensation. 

The  incidence  of  complications  of  this  kind  necessitate  the  free 
administration  of  cardiac  tonics  and  stimulants  so  long  as  there  is 
any  danger  of  failure  of  compensation,  in  addition  to  the  vigorous 
treatment  of  the  concomitant  affection. 

To  sum  up,  the  establishment  and  maintenance  of  compensation 
is  most  advantageously  secured  through  the  promotion  of  the  general 
health  by  means  of  the  intelligent  application  of  the  various  hygienic, 
dietetic  and  medicinal  measures  that  have  just  been  enumerated.  It 
is,  however,  a  great  mistake  to  suppose  that  the  best  results  in 
chronic  valvular  disease  are  obtained  by  the  rigid  application  of 
"hard  and  fast"  rules  of  treatment;  each  case  must  be  considered 
on  its  merits.  In  attempting  to  steer  between  the  Scylla  of 
cause,  and  the  Charybdis  of  effects  the  physician  must  turn  to 
account  all  those  conditions  of  constitution,  habits,  and  temperament 
which  operate  favourably,  and  ward  off,  counteract  or  minimize 
those  influences  which  act  prejudicially  on  the  health  of  the  patient 
in  general,  and  on  the  heart  and  vessels  in  particular.  Thus  the 
repression  of  excesses  does  not  mean  the  cultivation  of  asceticism 


238  DISEASES    OF   THE    HEART 

the  avoidance  of  fatigue  and  exhaustion  does  not  entail  the  adoption 
of  physical  and  mental  inactivity  and  slothfulness ;  it  is  between 
these  extremes,  into  the  paths  of  moderation,  that  the  lives  of 
those  suffering  from  chronic  valvular  disease  must  be  directed, 
and  it  is  only  by  an  intelligent  consideration  of  each  particular 
case  in  all  its  bearings,  that  this  result  can  be  attained. 


Treatment  after  Failure  of  Compensation. 

The  circulatory  equilibrium  established  by  the  most  perfect  com- 
pensation, though  stable  for  ordinary  requirements,  within  strictly 
moderate  limits,  cannot  be  maintained  in  the  face  of  sudden  or  pro- 
longed effort. 

Moreover,  the  existence  of  compensation  carries  with  it  certain 
difficulties  and  dangers,  which  are  partly  nutritional,  and  partly 
the  result  of  strain  on  the  heart  and  vessels.  These  forces,  assisted 
by  the  particular  tendency  to  interference  with  the  circulation,  both 
systemic  and  pulmonic,  that  is  associated  with  each  form  of  valvular 
disease,  are  a  constant  and  formidable  menace  to  the  maintenance 
of  compensation. 

Sooner  or  later  it  usually  happens,  as  the  result  either  of 
extrinsic  or  intrinsic  causes,  such  as  have  been  mentioned,  that 
compensation  breaks  down  and  dilatation  of  the  heart  from  failure 
supervenes. 

During  the  early  stages  of  this  process  the  discovery  and  removal 
of  the  cause  of  the  cardiac  insufficiency  will,  with  the  help  of  the 
treatment  hitherto  employed,  frequently  suffice  to  re-establish 
compensation  and  restore  the  balance  of  the  circulation. 

If,  however,  these  measures  fail  to  afford  the  requisite  amount 
of  relief,  or  if  the  cause  of  the  breakdown  cannot  be  discovered, 
or  is  irremovable,  the  failure  of  the  heart  must  be  combated  from 
the  side  of  its  effects. 

In  practice  the  two  methods  of  treatment  are,  as  a  rule,  employed 
together,  and  rightly  so,  since  the  one  is  the  complement  of  the 
other ;  but,  whenever  possible,  the  removal  of  the  cause  of  the 
cardiac  weakness  is  the  object  to  be  primarily  attained. 

Treatment  of  the  Cause. 

Dilatation  of  the  heart  from  failure  in  cases  of  compensated 
valvular  lesion  may  be  due  to  high  arterial  tension,  physical  or 
mental  overstrain,  worry  or  anxiety,  and  acute  intercurrent  disease, 
more  especially  rheumatism  and  pulmonary  disorders.  It  is  also 
commonly  brought  about  by  malnutrition  of  the  myocardium^  the 
result  of  insufficient  or  improper  food,  dyspepsia,  anaemia,  etc.,  and 
by  the  abuse  of  alcohol  and  tobacco. 

High  arterial  tension  can  be  reduced  and  kept  within  safe  limits 


CHRONIC   VALVULAR   DISEASE  239 

by  means  of  careful  dieting,  and  the  use  of  purgatives  and  other 
drugs  that  assist  in  the  ehmination  of  imperfectly  oxidized  waste 
products  from  the  blood. 

Nitrogenous  food,  in  the  form  of  meat  or  meat  extracts,  must 
be  used  in  strict  moderation,  and  should  not  be  taken  more  often 
than  once  a  day.  Plenty  of  fresh  air,  and  exercise  of  a  suitable 
kind  are  also  important  desiderata. 

A  mercurial  purge,  consisting  of  small  doses  of  calomel,  blue 
pill,  or  grey  powder,  should  be  administered  once  or  twice  a  week, 
and  may  be  followed,  after  a  few  hours'  interval,  by  a  draught 
of  some  saline  aperient,  preferably  the  sulphate  or  phosphate  of 
soda. 

The  salts  of  potash,  soda,  and  lithia  also  act  as  eliminating  agents, 
and  may  be  given,  as  occasion  demands,  in  conjunction  with  the 
measures  already  indicated. 

The  reduction  of  high  arterial  tension  may  be  rapidly  effected, 
during  an  emergency,  by  the  administration  of  vaso-dilators,  such 
as  nitro-glycerine,  nitrite  of  amyl,  etc.,  or  by  the  direct  abstraction 
of  blood. 

Failure  of  compensation  and  dilatation  of  the  heart  from  over- 
strain must  be  met  by  the  removal  of  the  cause  and  the  substitution 
of  complete  rest  so  long  as  there  are  any  symptoms  or  signs  either 
of  cardiac  irritability,  or  of  circulatory  disturbance. 

Exercise  should  be  resumed  with  as  much  care  as  if  compensation 
had  been  established  for  the  first  time. 

When  mental  overwork,  worry,  or  anxiety  is  suspected  as  the 
cause  of  the  cardiac  failure,  an  attempt  must  be  made  by  means 
of  change  of  air,  scenery,  and  surroundings  to  remove  or  minimize 
the  danger  arising  from  any  of  these  sources. 

The  treatment  called  for  by  the  incidence  of  acute  intercurrent 
disease  has  already  been  referred  to  in  the  section  deaUng  with 
the  maintenance  of  compensation. 

An  effusion  into  the  pleural,  pericardial,  or  peritoneal  cavity, 
occurring  as  a  complication  of  morbus  cordis,  requires  early  re- 
moval, since  the  strain  imposed  on  the  heart  by  the  accumulation 
of  even  a  small  quantity  of  fluid  in  any  of  these  situations  may 
give  rise  to  serious  embarrassment  of  the  organ. 

Dilatation  of  the  heart  from  failure  consequent  on  malnutrition 
of  the  myocardium  is  commonly  found  among  the  poorer  classes 
as  the  result  of  exposure,  insufficient  food,  or  insanitary  surround- 
ings. Compensation  is,  as  a  rule,  readily  restored  in  these  cases 
by  the  rest,  warmth,  and  wholesome  diet  that  can  be  obtained 
in  a  hospital. 

The  nutrition  of  the  heart  can  also  be  promoted  by  medicinal 
means.  Under  the  circumstances,  the  most  useful  drugs  for  this 
purpose  are  iron  and  arsenic,  which  may  be  given  alone  or  in 
combination  with  some  general  tonic  such  as  quinine,  strychnine 
or  phosphorus. 


240  DISEASES    OF   THE    HEART 

A  similar  plan  of  treatment  should  be  adopted  with  respect  to  the 
dilatation  of  the  heart  that  is  associated  with  anaemia. 

It  is  only  when  these  measures  fail  to  restore  compensation  that 
recourse  need  be  had  to  the  assistance  of  digitalis  or  other  cardiac 
tonics. 

The  treatment  of  the  malnutrition  of  the  heart  that  depends 
on  over-eating  and  drinking,  insufficient  exercise,  and  on  excesses 
of  various  kinds  must  commence  with  the  removal  of  the  cause. 
If  this  can  be  effected,  and  the  patient  is  prepared  and  able  to 
regulate  his  habits  and  mode  of  life  in  accordance  with  the  general 
principles  laid  down  in  the  previous  section,  the  restoration  of  com- 
pensation is  usually  only  a  matter  of  time. 

A  few  weeks'  complete  rest  in  bed,  in  conjunction  with  a  course 
of  massage,  forms  a  useful  preliminary  measure  in  the  treatment 
of  these  cases.  Care  must  be  taken,  when  exercise  is  resumed,  not 
to  overtax  the  heart. 

The  various  means  that  were  previously  recommended  for  the 
purpose  of  promoting  a  healthy  supply  of  blood  to  the  myocardium 
are  of  equal  service  in  the  treatment  of  the  cardiac  malnutrition 
that  is  due  to  the  causes  under  consideration. 

Considerable  benefit  may  also  be  derived  in  cases  of  this  kind 
from  the  method  of  treatment  devised  by  Dr.  Schott,  of  Nauheim, 
which  consists  in  the  use  of  still  or  aerated  baths,  and  carefully 
graduated  resisted  muscular  movements.  The  effect  of  the  baths 
and  exercises  on  the  heart  and  circulation  is  similar,  and  stated 
briefly  is  a  slowing  of  the  pulse  rate  with  an  increase  in  the 
volume  and  force  of  the  beat,  and  a  decrease  in  the  area  of  cardiac 
dulness,  i.e.,  an  improved  circulation  with  a  diminution  in  the  size 
of  the  heart. 

The  physiological  interpretation  of  these  results,  though  still  sub-' 
judice  is,  in  all  probability,  that  the  baths  and  resisted  exercises 
give  rise  to  dilatation  of  the  arterioles  of  the  skin  and  muscles 
respectively,  with  a  consequent  reduction  in  peripheral  resistance 
and  a  fall  of  mean  arterial  blood  pressure.  The  widening  of  the 
arteriolar  bed  in  the  skin  and  muscles,  as  the  case  may  be,  drains  the 
blood  from  the  venous  to  the  arterial  system^  and  more  particularly 
from  the  visceral  to  the  systemic  circulation.  The  heart  is  relieved, 
therefore,  both  on  the  arterial  and  on  the  venous  side  of  the 
circulation,  inasmuch  as  the  organ  is  contracting  against  diminished 
resistance  with  a  decreased  load.  The  fall  in  the  pulse  rate  is 
not  in  the  opinion  of  the  author  a  serious  objection  to  this  view, 
having  regard  to  the  condition  of  the  heart  and  circulation  which 
commonly  obtains  when  the  treatment  in  question  is  employed. 

Speaking  generally  the  subjects  of  mitral  disease  deserve  greater 
benefit  from  baths  and  resisted  movements  than  those  suffering 
from  aortic  lesions.  In  myocardial  affections  the  treatment  is 
sometimes  of  very  great  service.      Widespread  arterio-sclerosis  and 


CHRONIC    VALVULAR    DISEASE  24I 

advanced  cardiac  failure  are   contra-indications  to  the  employment 
of  this  form  of  treatment. 

Apart  from  the  method  that  has  just  been  considered,  the 
employment  of  massage  baths  and  needle  baths,  with  water  of  varying 
temperatures,  is  often  of  very  great  service  in  the  treatment  of 
failure  of  compensation  in  chronic  valvular  disease. 

Treatment  of  the  Effects 

The  disturbance  of  the  circulation  that  accompanies  failure  of 
compensation  and  dilatation  of  the  heart  is  directly  or  indirectly  the 
outcome  of  the  defective  driving  power  of  the  ventricles,  and  appears 
on  the  one  hand  as  arterial  anaemia,  and  on  the  other  as  venous 
congestion,  together  with  their  effects. 

The  attempt  to  relieve  these  conditions  and  to  restore  compensa- 
tion may  be  made  in  the  first  instance  from  the  side  of  the  circulation 
that  stands  in  the  greater  need  of  assistance. 

Thus  it  may  happen,  as,  for  instance,  in  cases  of  aortic  regurgita- 
tion when  asystole  threatens,  that  an  immediate  increase  in  the 
power  of  the  heart  is  urgently  required;  and  in  such  an  event 
free  stimulation  of  the  organ  offers  the  only  prospect  of  relief,  and 
must  be  employed  irrespectively  of  any  other  consideration.  On 
the  other  hand,  venous  engorgement  and  distension  of  the  right 
side  of  the  heart  may  become  so  great  that  failure  of  the  circulation 
is  an  imminent  danger,  and  in  this  case  assistance  can  be  rendered 
only  by  depletive  measures. 

As  a  general  rule,  it  is  preferable  to  reduce  cardiac  distension  and 
venous  engorgement,  and  diminish  the  work  of  the  heart  before 
increasing  the  force  of  its  contractions.  This  method  of  procedure 
has,  moreover,  many  practical  advantages,  and  it  will  be  adopted  in 
the  following  account  of  treatment. 

The  Reduction  of  the  Work  performed  by  the  Heart  in 
conjunction  with  the  Relief  of  Venous  Congestion 
and  of  the  Morbid  Conditions  associated  with  it. 

Rest,  more  particularly  complete  rest  in  bed,  constitutes  one 
of  the  most  available  and  powerful  means  of  reducing  the  work 
of  the  heart,  and  there  can  be  no  doubt  of  its  great  value  in  the 
treatment  of  valvular  disease  after  the  occurrence  of  failure  of  com- 
pensation. At  the  same  time,  the  rigid  enforcement  of  complete 
rest  must  be  tempered  by  tact  and  judgment,  since  strict  confine- 
ment to  bed  is  found  intolerably  irksome  by  some  patients,  whereas 
a  little  relaxation  in  the  observance  of  the  procedure  will  often 
enable  long  periods  of  inactivity  to  be  borne  with  comparative 
equanimity. 


242  DISEASES    OF   THE    HEART 

"■'Warmth  is  also  an  important  elem.ent  in  the  treatment,  for  by 
relaxing  the  cutaneous  vessels  it  facilitates  the  onward  flow  of 
blood,  and  thus  diminishes  the  work  of  the  heart.  Cold,  on  the 
other  hand,  by  contracting  the  superficial  arterioles,  adds  to  the 
difficulties  of  the  circulation. 

The  first  question  to  be  decided  in  the  treatment  of  cardiac  and 
venous  engorgement  is  whether  the  removal  of  blood  is  necessary 
for  its  relief.  If  the  distension  of  the  right  side  of  the  heart  is 
so  great  that  failure  of  the  ventricle  is  threatened,  there  can  be  no 
hesitation  in  the  abstraction  of  blood,  either  by  venesection  or  by 
leeches.  Venesection  should,  however,  not  be  employed  unless 
there  is  evidence  that  the  ventricular  muscle  is  sufficiently  powerful 
to  be  able  to  respond  to  this  sudden  mode  of  rehef.  It  is  not, 
as  a  rule,  necessary  to  remove  more  than  eight  or  ten  ounces  of 
blood,  and  this  can  be  most  conveniently  taken  from  one  of  the 
superficial  veins  of  the  arm. 

In  less  severe  cases,  as  well  as  in  those  instances  in  which 
venesection  is  inadvisable,  relief  can  usually  be  obtained  by  the 
use  of  leeches,  eight  or  ten  of  which  may  be  applied  over  the  pras- 
cordial,  or  preferably  the  hepatic  region. 

Irrespectively  of  the  employment  of  these  measures,  the  treatment 
of  cardiac  and  venous  engorgement  consists  in  the  administration 
of  purgatives  and  diuretics,  in  conjunction  with  cardiac  stimulants 
and  tonics. 

The  bowels  should  be  kept  freely  open,  at  first  by  means  of  calomel 
(gr.  i-iii)  and  compound  jalap  powder  (gr.  xx-xxx),  and  later  on 
by  small  doses  (gr.  i-iii)  of  calomel,  blue  pill,  or  grey  powder,  with 
rhubarb  or  colocynth,  which  may  be  given  at  night  two  or  three 
times  a  week  and  followed  next  morning  by  a  full  dose  of  a  saline 
aperient. 

The  beneficial  effect  of  free  purgation  on  the  engorgement  of  the 
portal  and  systemic  venous  circulations  is  greatly  increased  by  the 
diuresis  that  so  commonly  follows  the  relief  of  renal  congestion. 
The  action  of  the  kidneys  can  be  still  further  assisted  by  digitalis 
and  other  cardiac  tonics  which,  in  view  of  the  reduction  that  has 
been  effected  in  the  amount  of  work  that  is  required  of  the  heart, 
may  now  be  employed  with  advantage.  The  combination  of 
digitalis,  squill,  and  blue  pill,  or  of  digitalis  and  caffeine,  is  some- 
times of  great  service  in  promoting  diuresis.  The  salts  of  potassium, 
spirit  of  nitrous  ether,  etc.,  may  be  used  for  the  same  purpose. 

It  occasionally  happens  that  the  exhibition  of  diuretin  will 
promote  diuresis  after  the  failure  of  all  other  remedies.  The  drug 
should  be  given  in  ten  or  fifteen  grain  doses  every  three  or  four 
hours. 

It  is  sometimes  necessary,  while  relieving  the  heart  of  work,  to 
obtain  a  temporary  increase  in  the  force  of  the  cardiac  action,  and 
this  may  be  done  by  the  use  of  stimulants,  such  as  alcohol,  ether, 
ammonia,  or  strychnine.     On  the  other  hand,  a  transient  decrease  in 


CHRONIC    VALVULAR    DISEASE  243 

the  work  of  the  organ  may  be  effected  during  an  emergency  by 
means  of  nitroglycerine  and  the  nitrites  of  amyl  and  sodium,  etc., 
which,  by  dilating  the  arterioles,  lessen  peripheral  resistance. 

The  treatment  of  the  more  important  symptoms  and  morbid 
conditions  that  may  be  associated  with  venous  congestion  will  now 
be  briefly  considered. 

The  relief  of  the  dyspnoea,  which  depends  on  engorgement  of 
the  pulmonary  circulation,  can  be  obtained  only  by  the  measures 
that  have  hitherto  been  employed  in  the  treatment  of  venous  con- 
gestion. When  the  shortness  of  breath  is  aggravated  by  bronchitis, 
expectorants,  such  as  the  carbonate  of  ammonia,  squills,  senega, 
etc.,  should  be  added  to  the  other  remedies. 

The  inhalation  of  oxygen  is  also  of  service  by  relieving  the 
insufficient  aeration  of  the  blood. 

Paroxysmal  attacks  of  dyspnoea,  which  are  frequently  associated 
with  high  arterial  tension,  must  be  treated  by  free  stimulation 
of  the  heart  and  the  administration  of  nitrite  of  amyl  or  nitro- 
glycerine. 

Severe  and  continuous  dyspnoea,  which  cannot  be  relieved  by  the 
ordinary  methods  of  treatment,  is  sometimes  greatly  benefited  by 
the  hypodermic  injection  of  small  doses  (gr.  ^  to  ^)  of  morphia. 

Congestion  of  the  portal  circulation  is  usually  accompanied  by 
more  or  less  disturbance  of  digestion  ;  consequently  the  regulation  of 
the  diet  is  a  matter  of  the  first  importance.  There  is  no  objection 
to  solid  food  so  long  as  the  patient  can  digest  it,  but  sooner  or  later 
it  becomes  necessary  to  give  nourishment  wholly  or  partially  in  a 
liquid  form. 

The  treatment  of  dropsy  is  identical  with  that  of  venous  engorge- 
ment, and  consists  therefore,  in  the  use  of  diuretics  and  hydragogue. 
cathartics.  If  these  remedies  fail  to  afford  sufficient  relief,  the 
oedematous  tissues  may  be  drained  by  puncture  of  the  skin, 
which  should  be  done,  under  strict  antiseptic  precautions,  by  means 
of  Southey's  trochars- 

Effusion  into  any  of  the  large  serous  cavities  may  be  dealt  with 
by  paracentesis,  and  should  in  all  cases  be  dealt  with  promptly. 

Insomnia,  though  it  is  not  necessarily  a  consequence  of  venous 
congestion,  frequently  accompanies  the  disturbance  of  the  cerebral 
circulation  that  is  associated  with  failure  of  the  heart.  The  sleep- 
lessness is  sometimes  obviously  due  to  an  alteration  in  the  state  of 
arterial  tension,  but  as  a  general  rule  the  precise  circulatory  defect 
upon  which  it  depends  is  obscure. 

When  insomnia  is  due  to  high  arterial  tenson  it  can  be  readily 
relieved,  as  Sir  William  Broadbent  has  shown,  by  a  mild  mercurial 
aperient,  which  should  be  given  an  hour  or  two  before  sleep  is 
desired. 

The  sleeplessness  that  depends  on  low  systemic  tension  must  be 
treated  by  stimulants  and  cardio-vascular  tonics.  A  dose  of  caffeine 
at  night  will  often  produce  sleep  in  cases  of  this  kind. 


244  DISEASES    OF   THE    HEART 

Hypnotics,  of  which  sulphonal,  bromide  of  ammonium,  and 
paraldehyde  are  the  most  useful,  should  always  be  used  with  caution. 

Massage  is  frequently  of  service  in  the  treatment  of  the  insomnia 
that  is  due  to  circulatory  causes. 

When  other  means  fail,  sleep  can  often  be  obtained  by  the  sub- 
cutaneous injection  of  a  small  dose  (gr.  ^)  of  morphia. 


The  Increase  in  the  Power  of  the  Heart 

Stimulation  of  the  heart  by  means  of  alcohol,  ether,  the  salts  of 
ammonium,  or  strychnine  is  the  most  rapid  and  powerful  method 
of  temporarily  increasing  the  force  of  its  contractions.  In  con- 
ditions of  great  urgency  these  remedies  can  be  administered  sub- 
cutaneously.  Under  less  pressing  circumstances  half-drachm  doses 
of  ether  and  sal  volatile,  with  two  or  three  minims  of  hquor  strych- 
ninae,  may  be  given  by  the  mouth  every  two,  four,  or  six  hours, 
as  occasion  requires. 

Alcohol,  in  the  form  of  spirits,  is  a  very  convenient  and  powerful 
cardiac  stimulant,  and  it  possesses  the  additional  advantage  of  mixing 
well  with  most  of  the  ordinary  liquid  foods.  The  dose  must  be 
regulated  in  accordance  with  the  degree  of  stimulation  that  is  required. 
It  is  seldom,  if  ever,  necessary  to  prescribe  a  daily  allowance  of  more 
than  ten  or  twelve  ounces  of  alcohol,  which  should  be  taken  in  small 
quantities,  at  regular  intervals,  during  the  twenty-four  hours. 

The  application  of  hot  turpentine  stupes,  mustard  poultices,  or  a 
few  small  fly  blisters  to  the  prscordium,  and  of  pungent  substances 
to  the  nose,  are  also  of  service  in  stimulating  cardiac  action,  and  they 
may  be  employed  with  the  other  measures  that  have  been  men- 
tioned. An  increase  in  the  force  of  the  heart  of  a  more  durable 
quality  can  be  obtained  by  the  administration  of  the  so-called 
"  cardiac  tonics,"  of  which  digitalis  is  by  far  the  most  useful,  though 
other  members  of  the  group,  notably  strophanthus,  caffeine,  squill, 
convallaria,  sparteine,  etc.,  are  sometimes  of  very  great  service. 

These  remedies  may  be  given  with  ether,  the  salts  of  ammonium, 
or  strychnine,  or  with  iron,  arsenic,  nux  vomica,  phosphorus,  quinine, 
etc.,  according  to  the  special  needs  of  the  heart  and  the  general 
requirements  of  the  patient.  The  action  of  the  cardiac  tonics  is 
frequently  more  effective  when  two  or  three  are  used  together  than 
when  the  same  drugs  are  employed  separately  and  successively,  as 
may  be  observed  with  combinations  of  digitalis  and  caffeine  or 
squill,  and  of  strophanthus  and  convallaria  majalis.  Moreover,  this 
method  of  administration  is  in  all  probability  capable  of  considerable 
extension. 

A  purge  should  in  all  cases  precede  and  from  time  to  time  co- 
operate with  the  use  of  cardiac  tonics. 

The  physiological  action  of  digitalis,  which  will  be  taken  as  the 
type  of  the  remedies  under  consideration,  is  exerted  for  the  most 


CHRONIC   VALVULAR   DISEASE  245 

part  on  the  muscular  tissue  of  the  heart  and  arterioles.  Its  effect,  in 
moderate  doses,  is  to  increase  the  force  and  reduce  the  frequency  of 
the  cardiac  beats,  and  at  the  same  time  to  raise  the  tension  in  the 
arteries. 

The  indications,  therefore,  for  the  therapeutic  use  of  digitalis  are 
failure  of  the  heart  with  dilatation  of  its  cavities,  a  rapid,  weak,  and 
irregular  pulse,  venous  engorgement,  dropsy,  and  congestion  of  the 
viscera,  as  shown  by  dyspnoea  and  a  scanty  secretion  of  urine. 

Increased  functional  activity  of  the  kidneys,  a  diminution  of  the 
dropsy,  and  a  slower,  stronger,  and  more  regular  pulse  are  the  most 
reliable  manifestations  of  the  beneficial  action  of  the  drug. 

Strophanthus  is  a  useful  substitute  for  digitalis  when  the  latter 
drug  cannot  be  tolerated  or  has  failed  to  do  good.  The  precise 
conditions  for  the  successful  employment  of  this  remedy  have  not 
yet,  however,  been  fully  ascertained. 

The  action  of  convallaria  majalis  appears  to  be  very  uncertain,  but 
the  drug  is  sometimes  of  service,  more  especially  when  given  in 
combination  with  strophanthus. 

Sparteine  produces  a  prompt  but  temporary  increase  in  the  power 
of  the  heart,  consequently  it  may  be  used  with  strychnine  or  other 
cardiac  stimulants  in  order  to  tide  over  an  emergency. 

The  action  and  uses  of  digitalis  will  now  be  considered  in  greater 
detail. 

The  relief  afforded  by  the  drug  in  the  treatment  of  failure  of  the 
heart  and  its  effects  is  obtained  by  (i)  the  increase  in  the  contractile 
power  and  tone  of  the  cardiac  muscle,  whereby  the  ventricles  are 
enabled  to  more  completely  expel  their  contents,  while  the  size 
of  their  cavities  becomes  lessened;  (2)  the  lengthening  of  the 
diastole  of  the  heart  so  that  not  only  is  there  more  time  for  the 
nutrition  of  the  organ,  but  also  for  the  outflow  of  blood  from 
the  great  veins,  which  is  still  further  assisted  by  the  improved 
suction  power  of  the  stronger  ventricles  ;  and  (3)  the  rise  of  pressure 
in  the  arteries,  which  are  kept  better  filled  Ijy  the  more  vigorous 
ventricles,  whence  the  flow  of  blood  into  and  through  the  capillaries 
and  veins  is  maintained  at  a  more  rapid  and  regular  rate. 

The  diuretic  action  of  digitalis,  which  is  often  greatly  assisted 
by  the  co-operation  of  mercury  and  of  caffeine,  is  accounted  for  by 
the  rise  of  pressure  in  the  renal  arteries  and  the  consequent  improve- 
ment in  the  circulation  through  the  kidneys,  together  with  the  in- 
crease in  the  watery  constituents  of  the  blood  that  attends  the 
absorption  of  dropsical  effusions.  The  latter  circumstance  is  the 
most  powerful  factor  in  the  production  of  the  diuresis ;  for  in  the 
absence  of  dropsy  digitalis  has  but  little  influence  on  the  secretion  of 
urine. 

The  effects  of  digitalis  are  not  equally  serviceable  in  all  forms 
of  valvular  disease.  While  there  is  no  doubt  that  the  drug  is  of 
very  great  value  in  mitral  regurgitation,  whether  primary  or  secondary 


246  DISEASES    OF   THE    HEART 

to  other  valvular  lesions,  it  is  of  much  less  service,  and  at  times 
altogether  harmful,  in  mitral  stenosis,  and  in  aortic  incompetence 
and  aortic  obstruction. 

The  beneficial  influence  of  digitalis  in  mitral  regurgitation  is 
explained  by  the  increase  in  the  amount  of  contraction  of  the  left 
ventricle,  plus  the  decrease  in  the  size  of  its  cavity,  whereby  the 
auriculo-ventricular  opening  is  not  only  constricted,  but  is  also 
better  protected  (by  reason  of  the  closer  approximation  of  the 
valvular  curtains),  and  in  both  these  ways  the  leakage  through  the 
orifice  is  lessened.  Furthermore,  the  improvement  in  the  pulmonary 
circulation  consequent  on  the  increased  vigour  of  the  right  ventricle 
leads  to  a  larger  and  more  equable  supply  of  blood  to  the  left 
auricle,  and  hence  to  the  left  ventricle  and  aorta,  while  the  accom- 
panying rise  of  intra-auricular  pressure  assists  in  resisting  the  reflux 
through  the  mitral  opening.  It  is  of  course  to  its  efi'ects  on  the  right 
ventricle  and  pulmonic  circulation  that  the  beneficial  influence  of 
digitalis  in  mitral  regurgitation  is  chiefly  attributable. 

The  initial  effect  of  digitalis  in  mitral  stenosis  is  frequently 
beneficial,  and  is  due,  no  doubt,  to  the  prolongation  of  the  diastole 
of  the  heart  and  the  greater  power  of  the  right  ventricle,  whence 
more  time  is  allowed  for  the  discharge  of  the  auricular  contents, 
while  the  vis  a  tergo,  in  the  shape  of  heightened  pulmonic  tension,  is 
increased. 

The  subsequent  unfavourable  action  of  the  drug  is  explained  by 
Sir  William  Broadbent,  on  the  grounds  that,  so  soon  as  the  pressure 
in  the  pulmonic  circulation  and  left  auricle  has  reached  the  point 
at  which  the  blood  is  forced  through  the  narrowed  mitral  opening  at 
the  maximum  rate  of  speed,  further  stimulation  of  the  right  ventricle 
can  only  give  rise  to  embarrassment  of  the  organ. 

It  may  be,  too,  that  in  the  absence  of  hypertrophy  of  the  left 
ventricle,  the  increase  of  systemic  arterial  tension  offers  a  greater 
resistance  to  the  systole  of  the  heart  than  the  organ  is  able  to  cope 
with. 

When  digitalis  disagrees  in  cases  of  mitral  stenosis,  its  place  may 
be  taken  by  a  combination  of  strophanthus  and  convallaria  majalis, 
which  frequently  gives  surprisingly  good  results.  Since  this  com- 
bination exerts  comparatively  little  influence  on  arterial  tension,  it 
seems  probable  that  the  ill  effects  of  digitalis  in  mitral  stenosis  depend, 
to  some  extent  at  least,  on  vasomotor  changes.  If  incompetence  of 
the  mitral  valve  is  associated  with  narrowing  of  the  opening,  the 
effects  of  digitalis  will  be  beneficial  in  proportion  to  the  extent  of 
the  regurgitation. 

The  effects  of  digitalis  in  aortic  incompetence  will  be  harmful  in 
so  far  as  the  amount  of  backflow  is  augmented  by  the  rise  of 
arterial  tension  and  the  prolongation  of  the  diastole  of  the  heart, 
and  beneficial  in  so  far  as  the  dilatation  of  the  ventricle  is  reduced 
by  the  increase  in  the  contractile  power  and  tone  of  its  muscular 
walls. 


CHRONIC   VALVULAR   DISEASE  247 

Opinions  are  divided  with  regard  to  the  therapeutic  value  of 
digitahs  in  aortic  insufificiency,  for  while  some  observers  look  upon 
it  as  injurious,  others  consider  it  to  be  of  great  service  in  the  treat- 
ment of  this  disease.  Sir  WiUiam  Broadbent  suggests  that  these 
conflicting  views  can  be  explained  by  the  fact  that  the  influence  of 
digitalis  in  aortic  regurgitation  is  harmful  under  one  set  of  conditions 
and  beneficial  under  another.  Thus  if  the  failure  of  compensation 
in  aortic  incompetence  manifests  itself  predominantly  in  the  form  of 
arterial  anaemia,  digitalis  does  harm ;  whereas,  if  in  the  form  of 
mitral  backworking,  with  venous  congestion,  etc.,  it  does  good,  for 
the  reasons  given  under  the  head  of  "Mitral  Regurgitation." 

Be  this  as  it  may,  there  is  no  doubt  that  the  plan  of  procedure 
underlying  Broadbent's  suggestion,  forms  a  useful  and  practical 
working  rule  in  the  administration  of  digitalis  in  cases  of  aortic 
incompetence. 

It  sometimes  happens  that  a  combination  of  digitahs  and  strophan- 
thus  will  succeed  where  the  former  drug  alone  has  failed  to  be  of 
service. 

Aortic  stenosis  derives  most  benefit  from  digitalis  when  the  failure 
of  compensation  is  accompanied  by  evidence  of  backworking  through 
the  mitral  opening.  In  the  absence  of  mitral  leakage  digitalis  may 
do  harm,  in  that  it  increases  the  pre-existing  arterio-capillary  resist- 
ance and  thus  adds  to  the  work  of  the  left  ventricle. 

Strophanthus,  though  somewhat  uncertain  in  its  action  is  some- 
times of  very  great  service  in  the  treatment  of  aortic  disease.  The 
drug  may  be  given  in  combination  with  iron,  arsenic,  strychnine, 
etc.,  or  with  some  other  cardiac  or  general  tonic. 


CHAPTER    XXII 
DISEASES    OF   THE   MYOCARDIUM 


Classification — Section  I.  Hypertrophy  and  Dilatation  of  the  Heart ;  Definition  ; 
Classification  of  Kinds  of  Cardiac  Enlargement ;  Morbid  Anatomy  ;  Effects 
on  other  Organs  ;  Pathogenesis  ;  Etiology ;  Symptoms  ;  Physical  Signs ; 
Diagnosis;  Prognosis;  Treatment — Section  II.  Acute  Myocarditis;  Eti- 
ology ;  Morbid  Anatomy ;  Effects  on  the  Heart ;  Symptoms ;  Physical 
Signs ;  Diagnosis ;  Prognosis ;  Treatment — Section  HI.  Degenerative 
Diseases  of  the  Myocardium  ;  Definition ;  ^Etiology  ;  Morbid  Anatomy ; 
Pathogenesis  ;  Symptoms ;  Physical  Signs  ;  Diagnosis  ;  Prognosis  ;  Treat- 
ment— Section  IV.  Fatty  Diseases  of  the  Heart ;  Fatty  Infiltration ;  Fatty 
Degeneration — Section  V.  Fibroid  Disease  of  the  Heart — Section  VI. 
Growths  in  the  Heart. 

The  muscular  walls  of  the  heart  are  liable  to  be  affected  by  a 
variety  of  morbid  conditions,  which  for  descriptive  purposes  may 
be  arranged  as  follows  : — 

1.  Hypertrophy  and  Dilatation 

2.  Acute  Myocarditis 

3.  Degenerative  Diseases 

{a)  Parenchymatous,  etc. 

{b)  Fatty 

(c)  Fibroid  (including  cardiac  aneurism  and  chronic 
myocarditis) 

4.  Grov^^ths 

This  classification,  which,  from  a  pathological  point  of  view,  is 
far  from  exhaustive,  includes  nevertheless  the  greater  number  of 
affections  of  the  myocardium  that  are  of  cHnical  significance. 

Apart,  however,  from  hypertrophy  and  dilatation  of  the  heart,  the 
differential  diagnosis  of  myocardial  disease  is  usually  a  matter  of 
extreme  difficulty,  and  the  recognition  of  any  particular  lesion 
often  rests  as  much  on  the  general  state  of  the  patient  and  other 
causal  indications,  as  on  the  circulatory  phenomena.  The  reason 
for  this  is  that  we   are  at  present  unable   clinically  to   distinguish 

248 


DISEASES  OF  THE  MYOCARDIUM  249 

with  anything  like  precision  between  the  effects  of  different  morbid 
conditions  of  the  cardiac  walls,  since  all  tend  to  impair  the  muscular 
power  of  the  heart  and  thus  give  rise  to  the  signs  and  symptoms  of 
insufficiency  of  the  organ,  accompanied  by  mechanical  disturbance 
of  the  circulation. 


SECTION  I 

HYPERTROPHY  AND  DILATATION  OF  THE  HEART 

The  terms  "  hypertrophy  "  and  "  dilatation  "  as  apphed  to  the  heart 
are  used  to  distinguish  certain  processes  whereby  the  organ  increases 
in  size.     They  may  be  defined  as  follows  : — 

1.  Hypertrophy:  An  increase  of  the  muscular  tissue  of  the  heart 
which  leads  to  thickening  of  the  cardiac  walls  and  enlargement  of 
one  or  more  of  the  chambers  of  the  organ. 

2.  Dilatation  :  A  uniform  enlargement  of  one  or  more  of  the 
cavities  of  the  heart. 

Two  distinct  varieties  of  dilatation  are  recognised,  viz. : 

1.  Dilatation  from  the  overfilling  of  a  chamber  which  is  compensa- 

tory in  its  effect. 

2.  Dilatation  from  the  incomplete  emptying  of  a  chamber  which 

is  associated  with  failure  of  the  muscular  pov/er  of  the  heart. 

The  following  varieties  of  enlargement  of  the  heart  are  (after 
Dr  Mitchell  Bruce)  distinguished  as  the  result  of  the  operation 
of  one  or  more  of  these  processes. 

1.  Simple  hypertrophy  in  which  the   parietes   of  the  heart  are 

thickened  while  the  cavities  retain  their  normal  size. 

2.  Compensatory  dilatation  with  hypertrophy. 

3.  Simple  hypertrophy  with  dilatation  from  failure. 

4.  "Compensatory  dilatation  with  hypertrophy,"  with  dilatation 

from  failure. 

The  conditions  referred  to  under  numbers  2,  3,  and  4,  are  also 
known  as  "eccentric  hypertrophy"  and  "dilated  hypertrophy." 

In  all  of  them  the  capacity  of  one  or  more  of  the  chambers  is 
increased,  while  the  normal  thickness  of  the  walls  is  preserved  or 
augmented. 

At  the  same  time,  the  relative  proportions  of  hypertrophy  and 
dilatation  vary  greatly  in  different  cases. 

5.  Simple  dilatation  from  failure,  in  which  the  capacity  of  one 

or   more   of  the   cavities   is  increased,   while  the  walls  are 
diminished  in  thickness. 


250  DISEASES   OF   THE    HEART 

The  condition  formerly  described  under  the  term  "  concentric 
hypertrophy."  denoting  thickened  walls,  ^nth  diminished  size  of 
canities,  has  no  real  existence. 

Hypertrophy,  dilatation,  or  any  of  their  combinations,  may  be 
either  general  or  local;  that  is  to  say,  they  may  involve,  more  or 
less,  all  of  the  four  chambers  of  the  heart,  or  they  may  be  limited 
to  one  or  two  of  its  compartments. 

The  ventricles  are  more  frequently  the  seat  of  hypertrophy  than 
the  auricles,  and  the  left  side  of  the  heart  is  more  often  affected 
than  the  right.  This  order  reversed  expresses  the  liabiHty  of  the 
cardiac  cavities  to  undergo  dilatation. 

H}-pertrophy  and  dilatation  never  occur  as  primary  disorders. 
They  are  always  secondary'  to  some  other  affection,  and  the  import- 
ance of  this  fact  in  ,the  consideration  of  myocardial  disease  cannot 
be  too  strongly  insisted  upon. 

PATHOLOGICAL  ANATOMY 
Hypertrophy 

The  heart  appears  to  be  elongated,  more  especially  in  the  direction 
of  the  left  apex,  and  the  bulk  and  weight  of  the  organ  are  greater 
than  usual.  Increase  in  the  weight  of  the  heart  affords  the  most 
trustworthy  evidence  of  hypertrophy  that  we  possess.  Irrespective 
of  the  variations  produced  by  the  method  of  removal  that  is  adopted, 
the  average  weight  of  the  normal  heart  in  adult  males  ranges  be- 
tween II  and  13  ounces,  and  in  females  between  9  and  ii  ounces. 

The  walls  of  the  chambers  affected  by  hypertrophy,  predomi- 
nantly the  ventricles,  are  thicker  and  firmer  than  normal,  and  do  not 
collapse  on  section.  The  musculi  papillares  and  columnar  camese 
usually  participate  in  the  muscular  enlargement  of  the  heart.  Ex- 
cept in  the  case  of  the  left  ventricle,  pure  hypertrophy  of  the  cardiac 
walls  is  seldom  or  never  obser\-ed.  The  hypertrophied  muscle  fibre  is 
firm  and  of  a  brownish  red  colour,  becoming  bright  red  on  exposure. 

The  increase  in  bulk  of  the  muscular  tissue  is  chiefly  due  to  the 
formation  of  new  muscle  fibres.  Recent  researches  tend  to  show 
that  the  size  of  the  individual  fibres  is  slightly  increased,  otherwise 
the  histological  characters  of  the  myocardium  are  unaltered. 

Dilatation 

In  pure  dilatation  the  outline  of  the  heart  is  more  rounded  than 
normal,  and  the  weight  of  the  organ  is  never  increased.  The  en- 
largement of  the  affected  cavities  is  associated  with  thinning  of  their 
walls,  which  collapse  on  section. 

The  muscular  tissue,  which  may  be  firm  or  soft,  is  variously 
altered  in  colour.  Under  the  microscope  the  muscle  fibres  may 
present  a  normal  appearance,  but  more  often  they  are  either  the  seat 
of  inflammatory  changes,  or  in  some  stage  of  pigmentary,  granular, 
fatty,  or  fibroid  degeneration. 


DISEASES    OF   THE    MYOCARDIUM  251 

Hypertrophy  with  Dilatation 

This  association,  which  is  the  one  commonly  found  in  cases  of 
cardiac  enlargement,  combines  the  features  of  the  two  forms  just 
described,  i.e.  the  capacity  of  one  or  more  of  the  cardiac  chambers 
is  increased,  while  the  normal  thickness  of  the  walls  is  preserved  or 
augmented.  The  size  of  the  heart  is  always  increased,  while  the 
shape  of  the  organ  depends  on  the  relative  extent  of  the  two  asso- 
ciated changes.     The  weight  of  the  heart  is  greater  than  normal. 

The  muscular  walls  may  be  variously  altered  in  colour,  consist- 
ence, and  structure. 

ASSOCIATED    PATHOLOGICAL    CHANGES 

The  pathological  conditions  associated  with  hypertrophy,  dilata- 
tion,  or  any  of  their  combinations,  vary  with  the  site  and  nature  of 
the  primary  lesion.  In  the  large  majority  of  cases  disease  of  the 
valves  of  the  heart,  or  of  the  pericardium,  lungs,  or  kidneys,  is  the 
source  of  the  cardiac  enlargement.  Apart,  however,  from  the  primary 
pathological  conditions  that  may  be  found  in  association  with  cardiac 
enlargement,  hypertrophy  and  dilatation  give  rise  to  certain  changes 
in  the  heart  and  circulation  which  must  be  briefly  considered. 

The  increased  intra-cardiac  pressure  which  must  accompany  hyper- 
trophy, dilatation,  and  their  various  combinations,  leads,  sooner  or 
later,  to  more  or  less  thickening  of  the  valves,  chordae  tendinese, 
and  endocardium,  on  one  or  both  sides  of  the  heart.  The  arteries, 
both  systemic  and  pulmonic,  undergo  similar  changes  in  conse- 
quence of  the  additional  strain  to  which  they  are  exposed,  and  the 
subsequent  degeneration  of  the  thickened  walls  may  be  followed  by 
aneurism  or  rupture  of  the  affected  vessels.  Cardiac  and  venous 
thrombosis  are  sometimes  observed  in  the  later  stages  of  dilatation 
of  the  heart,  owing  to  the  slowing  of  the  circulation.  Portions  of 
the  thrombi  occasionally  become  detached,  and  the  liberated  frag- 
ments carried  by  the  blood  stream  may  give  rise  to  embolism  of  the 
arteries  of  the  heart,  lungs,  brain,  spleen,  kidneys,  etc. 

Pulmonary  embolism  is  very  commonly  the  result  of  systemic 
venous  thrombosis. 

Dilatation  from  failure,  whether  of  the  right  or  left  side  of  the 
heart,  leads  ultimately  to  a  further  series  of  changes,  which  culmi- 
nate in  general  venous  congestion  and  dropsy,  with  a  corresponding 
degree  of  arterial  anaemia. 

The  effect  of  this  process  on  the  other  organs  of  the  body  is 
firstly  disturbance  of  function,  and  later  the  production  of  organic 
lesions,  accompanied  by  fibrosis,  pigmentation,  atrophy,  etc.  The 
viscera  chiefly  aff"ected  are  the  lungs,  liver,  spleen,  alimentary  canal, 
kidneys,  brain,  and  heart. 

The  more  important  pathological  changes  which  are  found  in 
these  organs  may  be  briefly  summarised  as  follows : — 


252  DISEASES    OF   THE    HEART 

Lungs. — Pigmentation,  capillary  engorgement,  and  dilatation,  with 
more  or  less  interstitial  fibrosis  of  the  lungs,  constitute  the  chief 
effects  of  prolonged  mechanical  congestion.  These  changes,  which 
are  comprised  under  the  term  "  brown  induration  "  of  the  lungs,  are 
usually  associated  with  other  morbid  conditions,  such  as  pulmonary 
oedema,  and  collapse,  infarction,  pneumonia,  bronchitis,  and  emphy- 
sema. 

Liver. — The  liver  is  usually  enlarged,  but  in  cases  of  severe  and 
protracted  venous  congestion  it  may  become  reduced  in  size  as  the 
result  of  cyanotic  atrophy  with  cirrhotic  changes. 

The  cells  of  the  lobules  undergo  pressure  atrophy,  and  may  be 
observed  in  all  stages  of  pigmentary  and  fatty  degeneration.  The 
peculiar  mottling  of  the  organ  which  may  be  seen  on  section,  arises 
in  consequence  of  the  contrast  afforded  by  the  deep  congestion  of 
the  central  parts  of  the  lobules,  as  compared  with  the  lighter 
coloured  peripheral  portions,  and  has  given  rise  to  the  term  "nut- 
meg liver."  The  fibrous  stroma  of  the  liver  is  increased,  and  there 
is  usually  some  thickening  of  Glisson's  capsule. 

Spleen. — The  spleen  is  enlarged  in  the  early  stages  of  venous 
congestion,  and  shows  on  section  a  deep  purple  colour.  It  may 
subsequently  become  indurated  and  contracted.  Infarction  of  the 
spleen  is  of  common  occurrence. 

Stomach  and  Intestines. — The  sub-mucous  tissue  is  engorged 
with  blood,  and  the  mucous  membrane  usually  gives  the  appear- 
ances of  acute  or  chronic  catarrh.  Punctiform  haemorrhages  are 
also  frequently  observed. 

Kidneys. — The  kidneys  are  congested  and  enlarged,  and  they 
sometimes  show  cirrhotic  changes. 

Infarction  with  the  subsequent  production  of  depressed  cicatrices 
is  not  uncommonly  found. 

Brain. — The  brain  is  congested,  and  thrombosis  may  occur  in  the 
cerebral  veins  and  sinuses. 

Heart. — The  inter-muscular  connective  tissue  is  usually  increased, 
sometimes  greatly  so,  while  the  muscle  fibres  may  be  the  seat  of 
pigmentary,  granular,  or  fatty  changes. 

iETIOLOGICAL    PATHOLOGY 

Hypertrophy 

Cardiac  hypertrophy  is  in  all  cases  dependent  on  an  increase  in 
the  amount  of  work  required  of  the  heart,  and  its  occurrence  is 
explained  by  the  operation  of  two  physiological  laws,  which  are  : — 

I.  That  the  functional  activity  of  a  muscle  is  increased  by  tension 


DISEASES    OF   THE    MYOCARDIUM  253 

of  its  fibres.  Stated  in  other  words,  the  force  exerted  by  a 
muscle  in  its  contraction  is  (up  to  a  certain  maximal  limit) 
augmented  by  the  resistance  that  it  has  to  overcome,  i.e.  the 
greater  the  resistance  the  more  powerful  the  contraction. 
2.  That  if  a  muscle  is  the  seat  of  increased  functional  activity 
for  a  considerable  period  of  time  it  undergoes  hypertrophy, 
provided  it  has  an  adequate  nutritive  supply. 

The  work  done  by  the  cardiac  muscle  consists  in  the  propulsion 
forward,  from  an  auricle  into  a  ventricle,  or  from  a  ventricle  into 
an  artery,  of  a  certain  charge  of  blood.  If  the  resistance  to  the 
onward  flow  in  any  of  these  situations  be  abnormally  raised,  or  if 
the  charge  of  blood  be  unduly  augmented,  the  work  of  the  heart  is 
increased,  and  the  muscular  wall  of  the  chamber  on  which  the 
additional  stress  falls  will,  for  the  reason  given  above  (law  i), 
contract  more  forcibly  than  usual,  and  if  the  difficulty  persist,  will 
(law  2),  under  favourable  nutritive  conditions,  undergo  hypertrophy. 

The  conditions,  therefore,  under  which  cardiac  hypertrophy  is 
most  commonly  observed  are  affections  of  the  heart  itself,  such  as 
valvular  or  pericardial  disease,  and  disturbances  of  the  peripheral 
circulation  whereby  the  resistance  to  the  onward  flow  of  blood 
through  the  arteries  and  capillaries  is  abnormally  raised. 

Under  favourable  circumstances  the  degree  of  hypertrophy  evoked 
by  any  of  these  lesions  is  proportional  to  the  requirements  of  the 
occasion.  It  never  exceeds  this  amount,  though  it  not  infrequently 
falls  short  of  it. 

In  any  event  it  will  appear  that  hypertrophy  of  the  heart  does  not 
occur  as  a  primary  disorder,  but  is  always  secondary  to  and  depend- 
ent upon  some  other  disease,  the  evil  effects  of  which  it  removes  or 
minimizes.  The  adequacy  of  the  compensation  afforded  by  hyper- 
trophy in  cases  of  morbus  cordis,  is  gauged  by  the  extent  to  which 
the  normal  balance  of  the  circulation  is  restored.  Compensation 
may  be  regarded  as  perfect  when  the  circulatory  equilibrium  that  is 
re-established  by  hypertrophy  is  stable  within  ordinary  requirements, 
and  this  may  be  obtained  under  favourable  circumstances. 

Dilatation 

It  has  already  been  stated  that  dilatation  of  the  heart  is  of  two 
distinct  kinds,  viz.  that  due  to  overfilling  of  a  chamber  which  is 
compensatory  in  its  effect,  and  that  due  to  incomplete  emptying 
of  a  chamber  which  is  associated  with  failure  of  the  muscular 
power  of  the  heart.  Yet,  while  the  physiological  and  pathological 
significance  of  these  two  conditions  afford  a  striking  contrast,  the 
mechanical  processes  whereby  the  cardiac  dilatation  is  established 
in  either  event  are  practically  identical. 

In  both  cases  the  first  step  towards  the  production  of  dilatation 
of  the  heart  is  the  overcharging  and  consequent  distension  of  one 


254  DISEASES   OF   THE    HEART 

or  other  of  the  cardiac  chambers  with  blood.  The  increase  in 
capacil^,  which  most  be  supplied  in  order  to  accommodate  the 
additional  qoantitj  of  tdood,  is  obtained  by  the  yielding  of  the 
dastic  mnscolaT  panics  of  the  chamber  involved. 

Fiovided  the  causes  which  have  given  rise  to  this  enlaigement 
act  with  suOSkdoit  intoisity,  or  over  a  sufficiently  protracted  period 
of  time,  the  raTtliar  walls  become  permanently  stretched,  and  the 
cavity  they  encircle  becomes  jHnpoitionally  dilated. 

The  vital  phenomena  underlying  the  mechanical  process  just 
described  are  essentially  diffeieiit  for  the  production  of  the  two 
forms  of  dilatation  of  the  heart.  The  mode  of  development  of  the 
condition  in  each  case  will  now  be  con^dered  in  detaiL 

Dilatation  of  the  heart  from  overfilling  may  be  most  conveniently 
studied  in  connection  widi  the  cardiac  enlargement  that  attend[s 
amtic  regurgitation. 

In  this  disease  the  left  ventricle  during  diastole  receives,  in 
addition  to  the  normal  supply  from  the  left  auricle,  the  amount 
that  regurgitates  through  the  imperfecdy  clewed  aortic  opening. 
At  the  end  <tf  diastole,  therefore,  the  contents  of  the  ventricle 
exceed  the  normal  by  die  amount  of  the  aortic  reflux.  The  accom- 
modation of  the  overcharge  necessitates  an  increase  in  the  capacity 
of  the  Tentride;,  and  the  consequent  stretching  of  its  elastic  walls. 
EsjHessed  in  other  words,  the  forces  concerned  in  the  distension 
or  stretdiing  of  the  elastic  ventricular  waUs  during  diastole  are 
augmented  by  the  {Hessnre  that  is  exerted  by  the  backflow  of 
blood  from  die  aorta,  and  the  increase  in  the  capacity  of  the 
ijiambo-  is  the  expression  of  the  additional  distensUe  stress  to  which 
it  is  exposed.  This  condition  of  the  ventricle,  if  perpetuated, 
becomes  dilatation,  which,  as  has  been  shown,  is  due  to  overfilling. 

Pari  passu  widi  the  development  of  dilatation  the  ventricle 
undeigoes  hypoliophy,  by  reason  of  the  increased  work  entailed  in 
the  propulsion  of  a  greater  quantify  of  blood  than  usual.  The 
dilatation  of  the  left  ventride  is  as  much  a  part  of  the  compensatory 
artangemait  as  the  ccMicomitant  hypertrophy ;  for  so  long  as  the 
voitricular  ocHitiaction  is  carried  through,  the  normal  quantity  of 
blood  plus  the  amount  of  the  backflow  is  projected  into  the  aorta, 
and  thus  the  supply  to  die  sjirstemic  vessels  and  tissues  undergoes  no 
diminution. 

TTie  dilatation  of  the  left  ventricle  (associated  with  hypertroph} ) 
that  accompanies  mitral  regurgitation  is  also  the  n^ult  of  overfilling, 
and  is  compensatory  in  its  effect,  since  it  allows  for  the  mitral  reflux, 
and  at  the  same  time  permits  the  dischai^  of  an  adequate  supply  of 
blood  into  die  aorta. 

The  leascMiir^  employed  with  respect  to  enlargements  of  the  left 
ventricle  a{^lies  with  equal  force  to  oolaigements  of  the  right 
ventricle  under  corresponding  conditions. 

It  will  dius  appear  that  dilatation  of  a  cardiac  chamber  from 


DISEASES  OF  THE  MYOCARDIUM  255 

overfilling  is  always  the  result  of  a  valvular  defect,  and  that  it  is 
invariably  associated  with  hj-pertrophy. 

The  compensation  effected  is  due  {a)  to  the  dilatation,  in  so  far 
as  it  provides  for  the  amount  of  the  valvular  leakage,  and  thus 
prevents  any  diminution  in  the  supply  of  blood  to  the  systemic 
vessels,  and  (^)  to  the  hypertrophy,  in  so  far  as  it  enables  the 
ventricle  to  complete  its  contraction  and  to  expel  its  contents. 

Dilatation  of  the  heart  from  incomplete  emptying  may  be  con- 
trasted "with  dilatation  from  overfilling,  inasmuch  as  it  is  always 
the  result  of  failure,  either  absolute  or  relative,  of  the  cardiac 
walls,  and  consequently  entails  some  degree  of  disturbance  of  the 
circulation. 

The  mode  of  development  of  dilatation  of  a  cardiac  chamber 
from  incomplete  emptying  depends  on  the  co-operation  of  forces 
that  are  partly  mechanical  and  partly  vital,  and  it  is  the  introduction 
of  the  later  ^etiological  factor  which  renders  the  origin  of  the 
condition  one  of  considerable  complexity. 

In  order  to  illustrate  the  subject  it  will  be  convenient  to  treat 
of  the  left  ventricle  only,  but  it  must  be  understood  that  the 
reasoning  employed  is  of  general  apphcation  as  regards  the  other 
chambers  of  the  heart. 

Experimental  research  has  shown  that  at  the  end  of  the  ventricular 
systole  a  certain  quantity  of  blood  remains  in  the  upper  part  of  the 
chamber  between  the  valves  and  the  papillary  muscles. 

Any  increase  in  the  resistance  to  the  discharge  of  the  contents  of 
the  ventricle,  as  for  instance  a  rise  of  peripheral  tension,  adds  to 
the  amount  of  the  residual  blood,  which  can,  no  doubt,  vary 
considerably  within  the  physiological  limits  prescribed  by  the  degree 
of  reserve  power  possessed  by  the  heart.  So  long  as  this  restriction 
is  not  overstepped,  the  resulting  distension  of  the  ventricle,  neces- 
sitated by  the  accommodation  of  the  normal  charge  from  the  auricle, 
plus  the  residual  excess  of  blood,  may  be  termed  physiological. 

If,  however,  the  rise  of  peripheral  tension  persist,  or  be  raised 
above  physiological  limits,  or  if  the  muscular  power  of  the  heart, 
either  relatively  or  absolutely,  be  insufficient  for  the  adequate 
expulsion  of  the  ventricular  contents,  a  time  arrives  when  the 
contractile  energ}'  of  the  cardiac  walls  becomes  exhausted  before 
the  completion  of  the  systole.  A  certain  quantity  of  blood,  there- 
fore, which  ought  to  have  been  propelled  into  the  aorta  remains 
behind  in  the  chamber,  and  to  this  is  immediately  added,  for  the 
time  at  least,  the  normal  charge  firom  the  left  auricle.  Hence 
at  the  end  of  diastole  the  ventricle  is  overcharged  by  the  amount 
of  the  residual  excess  of  blood  left  by  the  preceding  incomplete 
systole.  The  accommodation  of  this  overcharge  necessitates  an 
increase  in  the  capacity  of  the  ventricle  and  the  consequent 
stretching  of  its  elastic  walls.  Moreover,  with  each  succeeding 
cardiac  cycle  the  ventricle  becomes  further  overloaded,  and  unless 


256  DISEASES    OF   THE   HEART 

the  cause    of  the    distension   is   removed   the    chamber    becomes 
permanently  enlarged,  or,  in  other  words,  dilated. 

If  the  causes  persist,  dilatation  once  established  tends  for  obvious 
reasons  to  increase ;  but  it  must  not  be  supposed  that  the  yielding 
of  the  cardiac  walls  is  gradual  and  continuous.  In  response  to 
the  additional  demands  made  upon  it,  the  ventricle  from  time  to 
time,  by  means  of  unusually  powerful  contractions,  succeeds  in 
temporarily  getting  rid  of  the  accumulation  of  blood  in  its  cavity; 
but  the  process  of  overloading  is  repeated,  and  step  by  step,  under 
the  influence  of  recurring  strain,  the  amount  of  dilatation  becomes 
greater.  In  advanced  cases  of  dilatation  from  failure  the  ventricle 
is  always  more  or  less  full  of  blood,  and  its  inflow  and  output  are 
reduced  to  very  small  dimensions. 

Under  circumstances  of  this  kind  the  slowing  of  the  circulation 
through  the  heart  favours  the  clotting  of  blood  in  its  cavities,  and  the 
consequent  formation  of  emboli  which  may  be  carried  to  distant  organs. 

The  production  of  dilatation  from  failure  depends  most  com- 
monly on  the  co-operation,  in  varying  degrees,  of  two  main  factors, 
either  of  which  may,  however,  occasionally  act  alone.  They  are 
(i)  an  increase  in  the  work  required  of  the  heart,  consequent  on 
augmented  arterio-capillary  resistance,  valvular  disease,  overstrain, 
etc.,  and  (2)  impairment  of  the  muscular  power  of  the  organ,  the 
result  of  structural  disease  of  the  cardiac  walls,  or  of  nutritive, 
neuro-muscular,  and  other  disturbances. 

Among  the  chief  morbid  conditions  of  the  myocardium  may  be 
mentioned  myocarditis,  fatty  and  fibroid  disease,  and  the  granular 
degeneration  of  the  muscle  fibres  that  accompanies  many  of  the 
acute  specific  fevers. 

Nutritive  disturbance  of  the  cardiac  walls  and  of  their  neuro- 
muscular apparatus  may  be  the  result  of  disease  of  the  coronary 
arteries,  rheumatism,  toxaemias  of  various  kinds,  anaemia,  dyspepsia, 
and  of  acute  and  chronic  pulmonary  disorders.  It  may  also  be  due 
to  a  large  number  of  other  causes  of  a  less  defined  influence,  but 
none  the  less  operative,  such  as  emotional  excitement  of  any  kind, 
anxiety,  grief,  worry,  and  nervous  overstrain,  more  particularly  in 
young  people.  It  is  possible,  too,  that  dilatation  of  the  heart  may, 
in  some  instances,  be  the  direct  effect  on  the  myocardium  of  poisons 
circulating  in  the  blood. 

The  abuse  of  tea,  alcohol,  and  tobacco,  dietetic  and  sexual 
excesses,  sedentary  and  irregular  habits,  chronic  constipation,  etc., 
are  also  contributory  factors  in  the  production  of  cardiac  dilatation. 

Acute  dilatation  of  the  heart  from  failure  is  sometimes  observed. 
Thus  it  may  occur  at  the  onset  of  acute  renal  disease,  especially 
when  this  disorder  is  associated  with  scarlet  fever.  Here  the 
increased  arterio-capillary  resistance,  combined  with  the  myocardial 
degeneration,  which  is  so  commonly  found,  leads  in  some  instances 
to  rapid  dilatation  of  the  left  ventricle. 

Acute  dilatation  of  the  heart  may  also  be  observed  in  the  course 


DISEASES    OF   THE    MYOCARDIUM         257 

of  many  of  the  acute  specific  fevers,  such  as  diphtheria,  measles,  enteric 
fever,  influenza,  etc.  It  may  Hkewise  be  due  to  sudden  or  excessive 
muscular  exertion,  and  to  poisoning  by  alcohol  and  other  drugs. 

Acute  dilatation  of  the  right  side  of  the  heart  is  seen  in  cases 
of  whooping  cough,  pulmonary  embolism,  over-exertion,  etc. 

Dilatation  from  failure  may  be  grafted  on  to  previous  enlarge- 
ment of  the  heart,  i.e.  on  to  hypertrophy,  or  on  to  dilatation  from 
overfilling  with  hypertrophy,  but  it  may  occur  without  any  ante- 
cedent increase  in  the  size  of  the  organ,  and  the  condition  is  then 
termed  primary  dilatation.  Any  or  all  of  the  cardiac  chambers 
may  be  the  seat  of  dilatation  from  failure. 

The  process  usually  commences  in  one  compartment,  and  grad- 
ually spreads  backwards,  chamber  by  chamber,  to  the  others  ;  so 
that  sooner  or  later,  as  the  case  may  be,  the  left  or  right  side  of 
the  heart,  or  the  whole  organ,  becomes  involved  in  the  morbid 
change.  The  mechanism  by  which  this  series  of  effects  is  produced 
has  already  been  described  under  the  head  of  "Mitral  Regurgitation," 
and  need  be  but  briefly  referred  to  here. 

Stated  shortly,  dilatation  of  the  left  ventricle  from  failure  leads  to 
incompetence  of  the  mitral  valve,  by  reason  of  the  inability  of  the 
stretched  and  weakened  muscle  fibres,  surrounding  the  auriculo- 
ventricular  orifice,  to  diminish  the  size  of  the  opening  sufficiently 
to  enable  the  valvular  curtains  to  come  into  adequate  apposition. 

Regurgitation  through  the  mitral  orifice  is  followed  by  dilatation 
of  the  left  auricle  and  a  general  rise  of  pressure  throughout  the 
pulmonary  circulation.  The  right  ventricle  subsequently  fails  before 
the  stress  of  driving  the  blood  through  the  lungs,  with  consecutive 
dilatation  of  the  tricuspid  opening  and  incompetence  of  its  valve. 
Tricuspid  regurgitation  is  followed  by  dilatation  of  the  right  auricle 
and  distension  of  the  veins  of  the  systemic  and  portal  circulations. 

The  further  effects  of  this  process  of  "  backworking  "  on  the  heart 
and  circulation  and  on  the  other  organs  of  the  body  have  been 
sufficiently  described  elsewhere. 

The  different  forms  of  cardiac  enlargement  that  have  been  de- 
scribed will  now  be  briefly  considered  with  reference  to  the  various 
ways  in  which  they  may  be  combined  and  associated. 

Hypertrophy  of  the  heart  seldom  occurs  in  a  pure  form,  but  it 
is  sometimes  seen  in  cases  of  aortic  and  renal  disease. 

Hypertrophy  of  the  heart,  with  dilatation  or  eccentric  hypertrophy, 
as  it  is  often  styled,  is  the  condition  most  commonly  found. 

Dilatation  of  the  heart  from  overfilling  is  most  typically  ex- 
emplified in  cases  of  aortic  regurgitation,  and  is  always  associated 
with  hypertrophy. 

Dilatation  of  the  heart  from  failure  may  supervene  on  either 
hypertrophy  or  on  dilatation  from  overfilling  with  hypertrophy,  or  it 
may  be  observed  without  any  previous  enlargement  of  the  organ. 

The  effect  of  hypertrophy,  and  of  dilatation  from  overfilling  with 
s 


258  DISEASES    OF   THE    HEART 

hypertrophy,  is  always  compensatory,  since  both  these  conditions 
counteract,  minimize,  or  remove  pre-existing  cardiac  disabihty. 

Dilatation  from  failure  is  invariably  the  result  of  inadequacy, 
either  absolute  or  relative,  of  the  muscular  power  of  the  heart,  and 
entails  some  degree  of  disturbance  of  the  circulation. 

All  or  any  of  the  cardiac  chambers  may  be  the  seat  of  enlarge- 
ment. As  a  rule  the  process  begins  in  one  compartment,  and 
spreads  backwards  to  the  others,  so  that  sooner  or  later  the  whole 
heart  is  involved.  It  is  by  virtue  of  this  backward  distribution  of 
the  effects  of  heart  disease  that  either  ventricle  is  enabled  to  come 
to  the  help  of  its  fellow. 

Thus  in  left-side  lesions  of  the  heart  the  backward  pressure 
through  the  mitral  opening,  left  auricle,  and  lungs  is  met  by  hyper- 
trophy of  the  right  ventricle,  which  by  maintaining  the  pulmonary 
circulation  ensures  an  adequate  supply  of  blood  to  the  left  auricle, 
and  hence  to  the  left  ventricle  and  aorta.  In  like  manner  the  left 
ventricle,  through  the  systemic  circuit,  comes  to  the  assistance  of 
an  overtaxed  right  heart. 

The  hypertrophy  of  the  left  ventricle  which  may  accompany  right- 
sided  lesions  of  the  heart  is,  in  part,  also  the  result  of  increased 
arterio-capillary  resistance  consequent  on  the  reflex  contraction  of 
the  small  arteries  through  the  vaso-motor  centre,  and  on  the  impedi- 
ment offered  by  the  arterioles  and  capillaries  to  the  circulation 
through  them  of  venous  blood. 

JETIOLOGY 

It  will  be  convenient  under  this  head  to  consider  the  causes  of 
enlargement  of  each  individual  cavity  of  the  heart  in  detail. 

LEFT  VENTRICLE 

Hypertrophy 

1.  Diseases  of  valves. — The  valvular  affections  which  induce 
hypertrophy  of  the  left  ventricle  are  aortic  stenosis,  aortic  incom- 
petence, and  mitral  incompetence. 

In  aortic  stenosis  the  hypertrophy  of  the  ventricle,  under  favour- 
able circumstances,  occurs  in  a  pure  form,  i.e.  it  is  not  associated 
with  dilatation.  In  aortic  and  mit^-al  incompetence  the  hypertrophy 
of  the  ventricle  is  combined  with  dilatation  from  overfiUing,  so  that 
in  both  instances  the  condition  known  as  eccentric  hypertrophy  is 
produced. 

2.  Diseases  of  the  aorta  and  its  branches. — The  affections  in- 
cluded under  this  heading  are  atheroma,  congenital  stenosis  of  the 
aorta,  and  aneurismal  dilatation  of  the  vessel. 

The  impairment  of  elasticity,  and  consequently  the  relatively  rigid 
condition  of  the  walls  of  the  aorta  and  systemic  arteries,  with  or 
without  narrowing  of  their  lumen,  that  is  occasioned  by  atheroma, 
not  only  offers  an  obstruction  to  the  blood  current,  but  also  directly 


DISEASES  OF  THE  MYOCARDIUM  259 

impedes  the  discharge  of  the  contents  of  the  ventricle,  which,  there- 
fore, undergoes  hypertrophy  from  increased  work. 

The  nutritive  conditions  associated  with  the  circumstances  under 
which  atheroma  is  observed  are,  however,  hardly  ever  satisfactory, 
hence  it  usually  happens  that  the  ventricular  hypertrophy  is  com- 
bined with  more  or  less  dilatation  from  failure. 

As  the  result  of  a  congenital  malformation,  the  aorta  is  sometimes 
found  constricted  just  beyond  the  point  of  entry  of  the  ductus 
arteriosus.  In  this  event  the  work  of  the  ventricle  is  increased, 
and  it  consequently  becomes  hypertrophied. 

Aneurism  of  the  aorta  may  or  may  not  give  rise  to  hypertrophy  of 
the  left  ventricle.  If  the  aneurism  involves  the  aortic  semilunar 
valve  hypertrophy  of  the  ventricle  is  the  rule,  whereas  it  is  the 
exception  if  the  valve  is  not  implicated.  The  ventricular  hyper- 
trophy is  associated  with  dilatation  from  overfiUing,  to  which  there 
is  frequently  added  dilatation  from  failure. 

3.  High  arterial  tension. — Next  to  valvular  disease,  the  most 
prolific  source  of  hypertrophy  of  the  left  ventricle  is  protracted 
high  arterial  tension.  This  condition  is  found  most  commonly 
in  association  with  acute  and  chronic  Bright's  disease,  especially 
contracted  granular  kidney,  gout,  lead  poisoning,  pregnancy,  and 
arterial  degeneration.  It  is  also  observed  in  some  cases  of  diabetes, 
anaemia,  and  emphysema,  and  not  infrequently  in  connection  with 
cardiac  neuroses  and  overstrain  of  the  heart.  In  some  instances 
an  hereditary  tendency  to  high  arterial  tension  has  been  noticed, 
and  in  any  event  the  liability  to  develop  the  condition  becomes 
more  pronounced  with  advancing  years. 

Among  the  more  important  predisposing  causes  of  high  arterial 
tension  may  be  mentioned  the  habitual  abuse  of  alcohol,  the  over- 
ingestion  of  nitrogenous  food,  constipation,  and  sedentary  habits. 

The  obstruction  to  the  free  passage  of  blood  through  the  small 
arteries  and  capillaries,  which  is  the  most  common  and  important 
factor  in  the  production  of  high  arterial  tension,  necessitates  an 
increased  display  of  force  by  the  left  ventricle  in  the  discharge 
of  its  contents,  so  that,  provided  it  enjoys  sufficient  nutrition,  the 
chamber  will  in  course  of  time  become  hypertrophied. 

The  hypertrophy  of  the  left  ventricle  due  to  high  arterial  tension 
is  observed  in  its  purest  form  in  cases  of  contracted  granular  kidney. 
In  many  cases,  however,  the  vigour  of  the  nutritional  forces  is 
insufficient  for  the  maintenance  of  adequate  hypertrophy,  and 
dilatation  from  failure  becomes  superadded. 

4.  Increased  functional  activity  from  prolonged  muscular 
exertion  or  from  nervous  excitation. — Hypertrophy  of  the  left 
ventricle  is  frequently  found  in  persons  whose  mode  of  life  entails 
severe  and  protracted  muscular  exertion.  Thus  it  occurs  among 
athletes,  hammer  men,  hill  climbers,  stonemasons,  and  among  those 
accustomed  to  carry  heavy  loads. 


26o  DISEASES   OF   THE    HEART 

In  such  instances,  the  cause  of  the  hypertrophy  which  is  physio- 
logical, is  twofold,  viz.  (i)  an  acceleration  in  the  rate  of  the  cardiac 
beat,  and  (2)  an  increase  in  the  peripheral  systemic  tension,  whereby 
the  work  of  the  heart  is  increased. 

In  cases  of  sudden,  violent,  and  prolonged  muscular  effort,  the 
Hmits  of  the  heart's  reserve  power  may  be  exceeded,  and  dilatation 
from  failure  results,  with  the  subsequent  production  of  hypertrophy, 
which  may  or  may  not  be  sufficient  to  restore  the  balance  of  the 
circulation. 

Acceleration  of  the  heart's  beat  does  not  necessarily  imply  in- 
creased work,  and  it  is  for  this  reason  that  the  rapidly  beating  heart, 
due  to  nervous  excitation,  does  not  undergo  hypertrophy,  unless 
associated  with  a  systemic  peripheral  tension,  which  is  above  the 
normal,  or  with  some  other  condition,  capable  of  giving  rise  to 
obstruction  to  the  blood  current. 

A  combination  of  muscular  exertion  and  nervous  excitation  is 
the  most  probable  cause  of  the  cardiac  enlargement  known  under 
the  name  of  "irritable  heart."  This  condition  has  been  most 
commonly  observed  among  soldiers  on  active  service,  a  mode  of 
life  which  entails  much  nervous  strain  and  excitement,  together 
with  severe,  sudden,  and  often  protracted  muscular  exertion.  The 
enlargement  of  the  heart  in  cases  of  this  kind,  though  commonly 
of  general  distribution,  affects  most  markedly  the  left  ventricle, 
which  shows  dilatation  in  association  with  a  variable  degree  of 
hypertrophy. 

The  mechanism  of  production  is  in  all  probability  an  initial 
dilatation  from  failure  and  the  subsequent  development  of  hyper- 
trophy, which,  owing  apparently  to  an  inherent  lack  of  cardiac 
reserve  force,  and  of  nutritional  vigour,  is  insufficient  to  completely 
counteract  the  effects  of  dilatation. 

Dilatation  of  the  heart,  it  may  be  pointed  out,  must  always  be  an 
indirect  cause  of  hypertrophy,  since  the  propulsion  of  the  additional 
quantity  of  blood  contained  in  the  enlarged  cavities  of  the  organ 
necessitates  an  increased  display  of  force. 

It  is  possible,  indeed  probable,  that  a  preliminary  distension  or 
even  dilatation  of  a  cavity  is  in  all  cases  the  immediate  precursor 
of  hypertrophy  of  its  walls. 

5.  Adherent  pericardium. — The  influence  of  pericardial  adhesions 
in  the  production  of  hypertrophy  of  the  left  ventricle  must  be 
ascribed  to  the  restraint  exercised  by  the  attachments  to  the  free 
movement  of  the  organ.  The  cardiac  hypertrophy  is  frequently, 
indeed  usually,  associated  with  dilatation  from  failure,  and  this  is 
especially  pronounced  in  the  case  of  the  right  ventricle  (see  p.  130). 

6.  Lesions  of  tlie  right  heart  and  obstructive  diseases  of  the 
lungs. — The  hypertrophy  of  the  left  ventricle,  which  may  accompany 
lesions  of  the  lungs  and  right  heart,  has  already  been  accounted  for 
in  a  preceding  section,  and  need  not  be  further  considered  here. 


DISEASES    OF   THE    MYOCARDIUM  261 

Dilatation 

Dilatation  of  the  left  or  right  ventricle  may  be  due  either  to  the 
overfilling  or  to  the  incomplete  emptying  of  their  cavities.  The 
mechanism  of  production  in  each  event  has  already  been  fully  con- 
sidered under  the  head  of  setiological  pathology. 

The  lesions  which  lead  to  dilatation  of  the  left  ventricle  from 
overfilling  are  aortic,  and  mitral  incompetence,  and  of  the  right 
ventricle,  pulmonic  and  tricuspid  incompetence. 

Dilatation  from  failure  is  the  result  of  either  the  absolute  or 
relative  inadequacy  of  the  contractile  power  of  the  ventricles  in  the 
face  of  the  resistance  that  they  have  to  overcome.  Thus  enfeeble- 
ment  of  their  muscular  walls  may  render  them  unequal  to  the 
ordinary  requirements  of  the  circulation,  or  the  work  to  be  done 
may  be  so  increased  that  even  the  healthy  cardiac  muscle  is  unable 
to  cope  with  it. 

An  increase  in  the  resistance  to  the  ventricular  contraction  is 
more  especially  operative  in  the  production  of  dilatation  from  failure 
when  the  additional  stress  occurs  suddenly,  as  well  as  with  con- 
siderable intensity. 

The  overstrain  of  the  heart,  under  such  circumstances,  may  be 
attended  with  a  serious  or  even  fatal  amount  of  dilatation. 

The  contractile  power  of  the  left  ventricle  may  be  enfeebled  by 
structural  disease  of  its  walls,  or  by  impairment  of  nutrition,  and 
by  toxemic,  nervous,  hereditary,  and  other  causes. 

The  resistance  to  be  overcome,  or,  in  other  words,  the  work  to  be 
accomplished  by  the  left  ventricle,  is  increased  by  any  of  the  con- 
ditions that  were  enumerated  under  the  causes  of  hypertrophy  of 
this  chamber. 

Provided  the  muscular  tissue  of  the  heart  is  sound,  and  its 
nutritional  vigour  unimpaired,  the  effect  of  an  increase  in  the  re- 
sistance to  the  onv/ard  flow  of  blood,  if  gradually  established,  is  to 
produce  hypertrophy  of  the  organ. 

The  subsequent  development  of  dilatation  from  failure,  if  it  occurs, 
is  explained  by  the  fact  that,  sooner  or  later,  the  nutritional  vigour 
of  an  hypertrophied  heart  tends  to  become  impaired  by  the  con- 
ditions under  which  hypertrophy  is  observed. 

On  the  other  hand,  if  the  cardiac  muscle  be  degenerated,  or  be 
suffering  from  any  form  of  malnutrition,  an  increase  in  the  resist- 
ance to  the  ventricular  systole,  however  gradual  its  occurrence,  is 
productive  of  dilatation  from  failure. 

Even  the  healthy  cardiac  walls  may  undergo  dilatation  from 
failure,  if  the  rise  of  the  intra-cardiac  pressure,  or  in  other  words 
the  increase  in  the  resistance  to  the  ventricular  systole,  be  sudden 
as  well  as  extreme.  In  such  cases,  however,  in  the  absence  of  a 
rapidly  fatal  termination,  a  variable  degree  of  hypertrophy  is  sub- 
sequently developed. 


262  DISEASES  OF  THE  HEART 


Acute  Dilatation 

It  will  be  convenient  under  this  head  to  briefly  consider  that  form 
of  acute  dilatation  of  the  heart  which  is  due  to  mechanical  strain. 

From  a  clinical  point  of  view,  the  effects  of  mechanical  strain  of 
the  heart  are  (i)  damage  to  the  orifices  and  valves  of  the  organ; 
(2)  damage  to  the  myocardium  ;  and  (3)  functional  disturbance  of 
the  heart.  It  is,  of  course,  obvious  that  these  results  are  more 
readily  produced  and  more  pronounced  when  the  valves  and  myo- 
cardium are  already  the  seat  of  malnutrition  or  morbid  changes. 

Apart  from  functional  disorders  of  the  heart  which  will  be  con- 
sidered later,  the  effects  of  acute  and  chronic  valvular  and  myocardial 
strain  have  for  the  most  part  been  described.  In  this  place  it  will 
be  necessary  only  to  call  attention  to  acute  parietal  strain  of  the 
heart  from  over-exertion  in  those  cases,  usually  young  subjects,  in 
which  the  organ  is  presumably  sound,  or  at  all  events  has  not 
previously  shown  any  appreciable  evidence  of  insufficiency. 

The  chief  interest  and  the  chief  difficulty  that  attach  to  acute 
parietal  strain  of  the  heart  are  the  manner  in  which  the  stress 
produced  by  violent  or  unwonted  exertion  tells  upon  the  organ. 
A  detailed  consideration  of  the  problem  is  out  of  the  question,  but 
an  attempt  will  be  made  to  briefly  outhne  the  chief  factors  concerned 
in  the  production  of  cardiac  stress  and  their  mode  of  operation. 

The  changes  in  blood  pressure  that  attend  muscular  exertion 
exercise,  of  course,  a  most  potent  influence. 

Active  muscular  exercise  raises  the  mean  arterial  blood  pressure 
at  the  outset,  and  subsequently,  at  a  variable  interval,  lowers  or 
even  annuls  the  rise.  The  duration  of  the  rise  of  the  mean  arterial 
pressure  varies,  according  to  Oliver,  with  the  nature  and  severity  of 
the  exercise,  and  with  the  vaso-motor  tone  of  the  individual,  etc. 

The  effect  of  exercise  on  the  venous  blood  pressure  is  similar; 
but  the  rise  of  pressure  is  somewhat  more  prolonged  than  on  the 
arterial  side  of  the  circulation.  Expressed  in  terms  of  heart  stress, 
the  initial  rise  of  blood  pressure  adds  to  the  work  of  the  left  ventricle 
in  proportion  to  the  extent  of  the  rise ;  the  subsequent  fall  of 
pressure  diminishes  the  work  of  the  ventricle.  The  rise  of  venous 
pressure  augments  the  supply  of  blood  to  the  right  side  of  the  heart, 
and  hence  by  way  of  the  lungs  and  left  auricle  to  the  left  ventricle. 
The  total  additional  work  imposed  on  the  left  ventricle  is  therefore 
the  propulsion  of  an  increased  charge  against  increased  resistance, 
while  in  the  case  of  the  right  ventricle  an  increased  charge  only  has 
to  be  dealt  with. 

The  influence  of  the  quickening  of  respiration  that  attends  all 
forms  of  muscular  exertion  is  difficult  to  gauge  with  anything  like 
precision.  Stated  generally,  inspiration  favours  the  diastolic  filling 
of  the  right  heart,  for  not  only  is  the  blood  aspirated  from  the  extra- 
thoracic  veins,  but  it  is  also  pressed  up  from  the  abdomen  by 
the   inspiratory  descent  of  the  diaphragm.     These  conditions  are 


DISEASES   OF   THE   MYOCARDIUM  263 

reversed  during  expiration.  Again,  so  far  as  the  pulmonic  circulation 
is  concerned,  inspiration,  when  the  breathing  is  rapid,  lessens  the 
supply  of  blood  to  the  left  heart,  while  expiration  increases  it.  The 
occurrence  of  dyspnoea  is  a  source  of  help  to  the  heart  and  circula- 
tion, inasmuch  as  each  respiration  pumps  blood  from  the  venous  side 
of  the  circulation  through  the  lungs  into  the  left  heart.  The 
general  effect  then  of  the  respiratory  pressures  that  attend  muscular 
effort  is  to  still  further  augment  the  supply  of  blood  to  the  right  and 
left  sides  of  the  heart,  and  in  this  way  to  increase  the  work  of  the 
ventricles.  Finally,  in  attempting  to  estimate  the  effects  of  pro- 
longed muscular  exertion  on  the  heart,  it  is  necessary  to  take  into 
consideration  the  influence  on  the  myocardium  of  the  nervous 
exhaustion  that  waits  upon  fatigue,  and  of  the  entrance  into  the 
circulation  of  the  waste  products  of  muscular  metabolism. 

It  will  appear,  therefore,  that  the  stress  imposed  on  the  heart  by 
muscular  exertion  consists  in  the  over-filhng  and  consequent  over- 
distension of  both  the  right  and  left  sides  of  the  organ.  The  left 
ventricle  has  also  to  contend,  initially,  against  increased  peripheral 
resistance.  Relief  to  the  left  ventricle  is  afforded  by  a  fall  in  blood 
pressure  consequent  on  diminished  peripheral  resistance,  and  to 
the  right  ventricle  by  increased  expansion  of  the  lungs,  which 
enlarges  the  bed  of  the  pulmonic  circulation,  and  by  the  safety-valve 
action  of  the  tricuspid  valve.  It  now  becomes  possible  to  roughly 
apportion  the  degree  and  kind  of  stress  to  which  each  side  of  the 
heart  is  exposed. 

Thus  at  the  outset  the  left  ventricle  has  to  cope  not  only  with  an 
increased  load,  but  also  with  increased  resistance  to  the  discharge 
of  its  contents.  Provided  the  limits  of  the  reserve  power  of  the 
heart  are  not  exceeded,  the  ventricle  is  able,  with  more  or  less 
difficulty,  to  propel  its  charge  of  blood  into  the  aorta.  The 
subsequent  fall  of  arterial  blood  pressure  enables  the  ventricle  to 
once  more  take  command  of  its  contents  and  carry  the  systole 
through. 

The  conditions  of  stress  on  the  right  side  of  the  heart  depend  for 
the  most  part  on  over-filling,  which  persists  during  prolonged 
muscular  effort  for  considerable  periods  of  time.  Distension  of  the 
right  ventricle  from  over-filling  is  a  normal  accompaniment  of  all 
forms  of  exertion,  and  is  no  doubt  a  cause  of  the  temporary  cardiac 
embarrassment  that  is  usually  experienced  by  most  individuals  during 
the  early  stages  of  unwonted  effort.  The  fall  of  pressure  in  the 
pulmonic  circulation  coincident  with  the  expansion  of  the  lungs,  and 
the  safety  valve  action  of  the  tricuspid  valve  enable  the  ventricle  to 
rise  to  the  occasion  and  deal  with  its  increased  charge,  so  that  the 
so-called  "  Second  Wind  "  is  established. 

These  then  are  the  effects  of  supportable  stress  on  the  heart  in  the 
normal  or  "  trained  "  subject. 

If  the  heart  "gives  out"  the  failure  may  occur  on  the  right  or  left 
side  or  on  both  sides  of  the  organ. 

In  cases  of  sudden  and  excessive  stress  the  left  ventricle  may  fail 


264  DISEASES   OF   THE    HEART 

to  completely  discharge  its  contents  with  each  systole,  so  that  the 
chamber  undergoes  dilatation  from  incomplete  emptying,  that  is, 
from  failure.  The  cause  of  the  cardiac  failure  in  these  cases  depends 
in  all  probability  on  interference  with  the  adjusting  vaso-motor 
mechanisms  which  make  for  a  reduction  in  blood  pressure.  Apart  from 
the  considerations  which  a  priori  lend  support  to  this  view,  the  chief 
argument  in  favour  of  it  is  the  fact  that  acute  dilatation  of  the  heart 
is  not  infrequently  observed  under  conditions  of  stress  which  seem 
totally  inadequate  to  explain  its  occurrence.  It  has  seemed,  too, 
that  this  event  is  more  especially  liable  to  occur  in  boys  of  a  nervous 
temperament. 

In  searching  for  an  explanation  of  the  apparent  anomaly,  it  may 
be  pointed  out  that  muscular  exertion,  more  particularly  among  boys, 
is  commonly  attended  by  emotional  excitement,  which  is  a  well 
attested  and  potent  source  of  increase  of  arterial  blood  pressure. 
It  is  this  factor  which  in  the  opinion  of  the  writer  has  not  been 
sufficiently  recognised  in  the  causation  of  acute  dilatation  of  the  left 
side  of  the  heart. 

Acute  dilatation  of  the  right  side  of  the  heart  may  be  contrasted 
in  respect  of  causation  with  the  similar  condition  on  the  left  side  of 
the  organ,  inasmuch  as  it  is  the  outcome  of  prolonged  muscular 
effort.  Allbutt,  who  originally  called  attention  to  the  effects  of 
mechanical  strain  of  the  heart,  believes  that,  to  all  intents  and 
purposes,  dilatation  of  the  right  side  of  the  heart  is  a  normal  incident 
of  prolonged  exertions. 

The  occurrence  of  acute  dilatation  of  the  right  heart  under  these 
circumstances  is  explicable  on  the  grounds  that  the  over-charging 
and  consequent  distension  of  the  ventricle  is  so  great  that  the 
chamber  is  unable  to  completely  discharge  its  contents  with  each 
systole,  and  consequently  undergoes  dilatation  from  incomplete 
emptying. 

This  event  is  more  likely  to  happen  when,  owing  to  an  insufficient 
increase  in  the  capacity  of  the  lungs,  the  resistance  in  the  pulmonic 
circulation  does  not  fall  enough  to  bring  the  work  of  the  ventricle 
within  the  limits  of  its  reserve  power. 

The  safety  valve  action  at  the  tricuspid  opening  must  in  the 
nature  of  the  conditions  that  obtain  quickly  become  exhausted,  so  far 
as  any  relief  to  the  right  ventricle  is  concerned.  No  doubt,  too,  in 
cases  of  prolonged  exertion  the  effects  of  the  waste  products  of 
muscular  metabolism  and  of  nervous  exhaustion  contribute  their 
quota  to  the  undoing  of  the  ventricle. 

It  is  doubtful  whether  a  heart  that  has  undergone  acute  dilatation 
ever  completely  recovers  its  tone  and  functional  vigour.  In  most 
instances,  at  all  events,  some  disability  is  left  behind  which  renders 
the  organ  unable  to  cope  with  stress  which  falls  well  within  the 
physiological  powers  of  a  normal  heart.  The  explanation  may  be 
that  interference  with  the  functional  capacity  of  an  organ  is  always 
productive  of  a  greater  or  less  degree  of  interstitial  fibrosis  which 
must  act  as  a  drag  on  functional  efficiency. 


DISEASES    OF   THE    MYOCARDIUM         265 

RIGHT  VENTRICLE 
Hypertrophy 

1.  Valvular   disease    on   the   right   side   of    the   heart. — The 

valvular  diseases  which  give  rise  to  hypertrophy  of  the  right 
ventricle  are  pulmonary  stenosis  and  pulmonary  incompetence, 
and  tricuspid  insufficiency,  as  well  as  any  combinations  of  these 
lesions.  The  mode  of  production  of  the  ventricular  hypertrophy 
resembles  in  all  respects  that  described  for  the  corresponding 
affections  on  the  left  side  of  the  heart.  Hypertrophy  of  the  right 
ventricle,  except  in  cases  of  pulmonary  stenosis,  is  usually  attended 
with  a  considerable  degree  of  dilatation. 

2.  Valvular  disease  on  the  left  side  of  the  heart. — The  rise  ot 
pressure  in  the  pulmonary  circulation  induced  by  mitral  and  even- 
tually by  aortic  lesions,  necessitates  an  increase  in  the  work  of  the 
right  ventricle,  which  consequently  undergoes  hypertrophy. 

Mitral  disease,  predominantly  mitral  stenosis,  is  more  efficacious 
in  this  respect  than  aortic. 

The  hypertrophy  of  the  ventricle  is  seldom  found  in  a  pure  state, 
that  is  to  say,  it  is  usually  combined  with  dilatation  from  failure. 

3.  Diseases  of  the  lungs. — The  pulmonary  affections  which 
interfere  with  the  passage  of  blood  from  the  right  to  the  left  side 
of  the  heart,  and  thus  increase  the  work  of  the  right  ventricle  and 
give  rise  to  its  hypertrophy,  are  chiefly  bronchitis,  and  emphysema, 
consolidation,  collapse,  and  fibrosis  of  the  lungs. 

The  ventricular  hypertrophy  is  almost  always  associated  with 
more  or  less  dilatation  from  failure,  w^hich  in  many  cases  is  the 
primary  lesion. 

4.  Adherent  pericardium. — The  effect  of  pericardial  adhesions 
in  the  production  of  cardiac  enlargement  is  more  marked  in  the 
case  of  the  right  ventricle  than  of  the  left.  The  reasons  for  this 
are  that  the  comparatively  thin  walls  of  the  right  ventricle  suffer 
more  from  the  primary  inflammation  and  are  less  capable  of  resist- 
ance than  the  thicker-walled  left  ventricle,  and  further,  that  the 
fibrous  attachments  act  over  a  relatively  large  superficial  area  in 
the  case  of  the  former  chamber  as  compared  with  the  latter. 

Dilatation  from  failure  is  always  associated  with  the  ventricular 
hypertrophy,  and  is  not  infrequently  the  predominant  condition. 

Dilatation 

The  right  ventricle  is  more  liable  to  undergo  dilatation  from 
failure  than  the  left.  This  is  accounted  for  by  the  proportionately 
diminished  power  of  resistance  to  strain  possessed  by  the  thinner 
walls  of  the  right  ventricle,  and  also  by  the  fact  that  the  nutritive 


266  DISEASES   OF   THE   HEART 

processes  associated  with  the  conditions  under  which  the  chamber 
is  exposed  to  stress,  are  seldom  favourable  for  the  production  or 
maintenance  of  an  adequate  degree  of  hypertrophy. 

The  explanation  given  of  the  mode  of  production  of  dilatation 
of  the  left  ventricle  applies,  mutatis  mutafidis,  with  equal  force  to 
the  right. 

All  the  causes  of  hypertrophy  of  the  right  ventricle  lead,  sooner  or 
later,  to  dilatation  of  the  chamber  from  failure.  Dilatation  of  the 
right  ventricle  from  overstrain  consequent  on  severe  and  prolonged 
muscular  effort  is  by  no  means  uncommon,  and  in  extreme  instances 
a  rapidly  fatal  termination  is  sometimes  observed  on  account  of  the 
supervention  of  asystole. 

LEFT    AURICLE 
Hypertrophy 

The  most  common  cause  of  hypertrophy  of  this  chamber  is  mitral 
stenosis,  in  which  disease  the  thickness  of  the  auricular  walls  has 
been  known  to  exceed  one  quarter  of  an  inch.  The  hypertrophy  of 
the  auricle  is  usually  accompanied  by  a  variable  degree  of  dilatation 
from  failure. 

Hypertrophy  in  association  with  dilatation  is  observed,  also,  in 
cases  of  mitral  regurgitation. 

Dilatation 

Dilatation  of  the  left  auricle  accompanies  all  forms  of  mitral 
disease,  whether  obstructive  or  regurgitant. 

RIGHT  -AURICLE 

Hypertrophy 

Hypertrophy  of  the  right  auricle,  with  dilatation,  is  seen  in  cases 
of  tricuspid  stenosis  and  of  primary  incompetence  of  the  valve. 

Dilatation 

Insufficiency  of  the  tricuspid  valve,  in  whatever  manner  produced, 
or  narrowing  of  the  opening,  leads  to  dilatation  of  the  right  auricle. 


SYMPTOMS 

Hypertrophy 

So  long  as  hypertrophy  is  efficient,  that  is,  so  long  as  there  are  no 
indications  of  embarrassment  of  the  circulation,  or  of  respiratory 
distress  or  disturbance,  during  rest  or  moderate  exertion,  symptoms 


DISEASES   OF   THE    MYOCARDIUM         267 

are  few  and  unimportant.  A  feeling  of  fulness,  uneasiness,  con- 
striction, or  pressure,  amounting  in  some  instances  to  actual  pain, 
may  be  experienced  in  the  praecordial  region. 

Palpitation  of  the  heart  is  easily  excited,  and  may  be  accom- 
panied by  rapid  or  irregular  action  of  the  organ.  A  dry,  irritating 
cough,  with  or  without  a  sense  of  respiratory  oppression,  is  some- 
times a  source  of  much  discomfort. 

Throbbing  sensations  in  the  head  and  neck,  noises  in  the  ears, 
vertigo,  or  muscse  volitantes  may  be  complained  of,  especially  after 
unusual  muscular  or  mental  effort.  Sleeplessness  is  sometimes  a 
troublesome  symptom. 

Epistaxis,  hemoptysis,  hsematemesis  or  melsena,  and  cerebral 
hsemorrhage  may  occur  as  the  result  of  arterial  rupture,  consequent 
on  the  strain  to  which  these  vessels  are  exposed  in  cases  of  cardiac 
hypertrophy. 

Other  symptoms  which  may  be  observed  are  due  less  to  the  hyper- 
trophy of  the  heart  than  to  the  causes  that  have  given  rise  to  it. 

The  earliest  indication  of  commencing  failure  of  compensation  is 
the  occurrence  of  dyspnoea  on  slight  provocation,  but  it  must  be 
borne  in  mind  that  the  presence  of  this  symptom,  without  other 
evidence,  is  no  proof  of  the  existence  of  heart  disease. 

Dilatation 

It  will  be  advantageous  to  trace  the  symptoms  which  attend 
dilatation  from  failure  in  the  order  of  their  usual  occurrence,  from 
the  left  to  the  right  side  of  the  heart,  and  from  the  time  when  failure 
of  compensation  begins. 

During  the  early  stages  of  the  process  the  patient  complains  of 
shortness  of  breath  on  slight  exertion,  accompanied  by  prsecordial 
uneasiness  or  pain,  palpitation  and  irregular  action  of  the  heart. 
The  imperfect  supply  of  blood  to  the  brain  gives  rise  to  lassitude, 
headache,  drowsiness,  or  sleeplessness,  and  attacks  of  giddiness  or 
faintness. 

Digestive  derangements,  manifested  by  a  furred  tongue,  loss  of 
appetite,  nausea,  pain  after  food,  flatulence,  and  irregular  action  of 
the  bowels  are  among  the  earliest  indications  of  commencing  failure 
of  compensation.  Flatulent  distension  of  the  stomach  may  be  a 
source  of  great  discomfort,  or  even  of  danger,  by  reason  of  the 
interference  with  the  free  action  of  the  heart.  The  development  of 
mitral  incompetence  leads  to  a  general  aggravation  of  the  symptoms. 
The  shortness  of  breath  becomes  more  pronounced  and  more  easily 
excited,  and  is  now  attended  by  cough,  haemoptysis,  and  the  signs 
of  engorgement  of  the  pulmonary  circulation.  "^ 

The  appearance  of  the  patient  at  this  stage  of  the  disease  is  often 
highly  suggestive  of  imperfect  aeration  of  the  blood.  Thus  the 
cheeks,  lips,  nose,  and  ears  present  a  dusky  bluish  red  or  ashy  hue ; 
the  hands  and  feet  are  cold  and  livid.     Nutrition  is  seriously  inter- 


268  DISEASES  OF  THE  HEART 

fered  with,  and  the  heart  suffers  in  common  with  the  other  organs 
of  the  body,  to  the  detriment  of  the  compensatory  changes  and  of 
the  patient  generally. 

A    Wasting  may  be  observed,  more  especially  in  the  case  of  children. 

^    Failure  of  the  right  heart  is  followed  by  a  further  series  of  events, 

which  culminate  in  portal  and  systemic  venous  congestion  and  dropsy. 

Shortness  of  breath,  which  may  amount  to  orthopnoea,  is  now  a 
constant  and  distressing  symptom. 

The  congestion  of  the  portal  circulation  leads  to  further  functional 
derangement  of  the  liver,  stomach,  and  intestines,  with  the  pro- 
duction of  jaundice,  persistent  dyspepsia,  and  constipation  or 
diarrhoea. 

The  urine  is  high-coloured,  diminished  in  quantity,  and  shows  on 
standing  a  copious  deposit  of  urates.  It  usually  contains  albumen 
and  occasionally  blood. 

Dropsy  commences  in  the  feet  and  gradually  spreads  upwards. 
The  loose  cellular  tissues  of  the  scrotum  and  lumbar  region  are  often 
enormously  distended  with  fluid.  Dropsical  effusion  may  also  take 
place  into  the  serous  cavities  of  the  pleurae,  pericardium,  and 
peritoneum,  events  which  add  greatly  to  the  cardiac  embarrass- 
ment. 
^  '  'Haemorrhages  sometimes  occur  into  the  subcutaneous  tissues,  and 
the  oedematous  skin  may  be  the  seat  of  erysipelatous  inflammation, 
or  even  of  gangrene. 

Epistaxis,  hsematemesis,  or  m.eljena,  menorrhagia,  etc.,  are  ob- 
served as  the  result  of  venous  or  capillary  rupture. 

The  signs  and  symptoms  of  the  embolic  plugging  of  one  of  the 
arteries  of  the  spleen,  kidneys,  brain,  or  lungs  may  appear  at  any 
stage  of  the  disease. 

Death  is  usually  due  to  a  process  of  slow  asphyxia  dependent  on 
the  gradual  enfeeblement  of  the  cardiac  walls.  The  fatal  termina- 
tion is  sometimes  precipitated  by  an  acute  pulmonary  or  pericardial 
complication,  or  by  some  accidental  circumstance,  such  as  embolism 
of  a  cerebral  artery,  etc. 

Excluding  valvular  affections,  sudden  death  is  rarely  observed, 
except  as  the  occasional  result  of  fatty  disease  of  the  myocardium, 
or  extensive  pericardial  adhesions. 

In  cases  of  primary  tricuspid  regurgitation,  and  of  disease  of  the 
right  ventricle,  affecting  that  chamber  exclusively  or  predominantly, 
Sir  William  Broadbent  has  observed  (Lumleian  Lectures,  1 891)  that 
the  symptoms  have  been  due  rather  to  an  insufficient  supply  of 
blood  to  the  left  ventricle,  giving  rise  to  a  tendency  to  syncope,  than 
to  damming  back  of  blood  in  the  veins. 

The  symptoms  of  acute  dilatation  of  the  heart  are  sudden  acute 

/pain,  or  a  feeling  of  great  oppression  or  of  something  giving  way  in 

the  chest,  accompanied  by  pallor  of  the  face,  collapse,  sweating,  rapid 

shallow   breathing,  or   a   peculiar   gasping  respiration,  restlessness, 

delirium,  together  with  coldness  and  lividitv  of  the  extremities. 


DISEASES  OF  THE  MYOCARDIUM  269 

PHYSICAL  SIGNS 

HYPERTROPHY  OF  THE  LEFT  VENTRICLE 

There  is  nothing  particularly  characteristic  about  the  appearance 
of  patients  suffering  from  hypertrophy  of  the  heart,  apart  from  the 
conditions  that  have  given  rise  to  it. 

The  pale,  puffy  face  of  Bright's  disease,  or  the  greyish-white  com- 
plexion associated  with  aortic  lesions,  could  not  fail  to  strike  the 
observer  in  a  case  of  cardiac  hypertrophy,  of  which  either  of  these 
affections  was  the  cause. 

Pulse 

The  character  of  the  pulse  varies  with  the  condition  which  has 
given  rise  to  the  hypertrophy. 

In  high  arterial  tension  the  artery,  which  may  be  small  or  large, 
is  full  between  the  beats,  and  can  be  rolled  beneath  the  finger ;  the 
pulse  wave  rises  and  falls  slowly,  and  is  not  easily  obliterated  by 
pressure.  The  coats  of  the  vessel  may  be  normal,  but,  as  a  rule, 
they  are  more  or  less  thickened  and  distorted. 

Extensive  fibroid  degeneration,  with  loss  of  elasticity  of  the 
arterial  walls,  will  modify  the  characters  of  the  pulse  :  for  although 
the  vessel  still  remains  full  between  the  beats,  the  wave  now  rises 
and  falls  quickly. 

In  aortic  incompetence  the  artery  is  large,  empty  between  the 
beats,  and  the  pulse  wave  rises  and  falls  abruptly,  giving  the  peculiar 
sensation  of  collapse  so  characteristic  of  this  affection. 

In  aortic  stenosis  the  artery  is  small,  and  can  be  felt  between  the 
beats;  the  pulse  wave  rises  and  falls  slowly,  and  is  not  easily 
obliterated  by  pressure. 

The  pulse  of  mitral  regurgitation  is  irregular,  both  in  force  and 
frequency,  while  the  artery  is  of  variable  size,  and,  as  a  rule,  cannot 
be  felt  between  the  beats. 

Heart 

Inspection. — There  may  be  prominence  or  even  bulging  of  the 
prsecordial  area.  This  is  most  commonly  observed  in  the  case  of 
children,  whose  chest  wall  is  softer  and  more  capable  of  yielding 
than  that  of  adults. 

The  apex  beat,  if  visible,  is  seen  to  be  displaced  downwards  and 
somewhat  outwards,  and  may  be  situated  in  the  sixth  or  seventh 
intercostal  space,  or  even  lower.  Systolic  retraction  of  the  inter- 
costal spaces  immediately  above,  and  internal  to  the  apex  beat, 
is  occasionally,  though  rarely,  observed. 

The  impulse  of  the  ventricle  is  a  deliberate  circumscribed  push 
or  heave,  frequently  strong  enough  to  visibly  raise  the  chest  wall. 

Pulsation  may  be  observed  in  the  carotid  arteries  of  the  neck, 
more  especially  in  the  case  of  aortic  regurgitation. 


270  DISEASES  OF  THE  HEART 

Palpation. — The  position  of  the  apex  beat  can  now  be  exactly 
determined  by  the  finger. 

The  impulse  of  the  ventricle  is  felt  as  a  prolonged,  powerful, 
localized  thrust. 

Pulsation  may  be  detected  immediately  to  the  right  of  the 
sternum,  in  the  first  and  second  interspaces,  when  dilatation  of  the 
aorta  is  associated  with  hypertrophy  of  the  left  ventricle.  The 
character  of  the  ventricular  impulse  may  be  masked  by  overlapping 
lung  in  cases  of  emphysema. 

Percussion. — The  area  of  cardiac  dulness  is  increased  downwards 
and  to  the  left. 

Auscultation. — At  the  apex  the  first  sound  is  duller  and  more 
prolonged  than  normal,  probably  because  the  muscular  element 
of  the  first  sound  now  predominates  over  the  valvular.  In  the 
absence  of  aortic  valvular  disease,  the  second  sound  at  the  apex 
is  usually  more  or  less  accentuated. 

Persistent  redupHcation  of  the  first  sound  of  the  heart  is  indica- 
tive of  commencing  failure  of  the  left  ventricle. 

At  the  base  over  the  aortic  cartilage,  the  first  sound  is  indistinct, 
or  altogether  inaudible;  the  second  sound  is  heard  louder  than 
normally.  If  the  root  of  the  aorta  is  dilated  the  second  sound 
is  not  only  accentuated,  but  has  in  addition  a  low-pitched  ringing 
quality. 

The  association  of  a  weak,  indistinct  aortic  second  sound  with 
high  arterial  tension  and  a  vigorous  hypertrophied  ventricle  strongly 
suggests  the  coexistence  of  aortic  valvular  disease. 

The  adventitious  auscultatory  phenomena  which  attend  h}'per- 
trophy  and  dilatation  of  the  heart  in  cases  of  valvular  disease  have 
been  described  elsewhere,  and  will  not  be  reconsidered,  otherwise 
than  incidentally,  in  this  section. 

DILATATION  OF  THE  LEFT  VENTRICLE 

Physiognomy 

The  subjects  of  cardiac  dilatation  present,  sooner  or  later,  the 
appearances  described  under  the  head  of  mitral  regurgitation.  In 
advanced  cases  the  patient  exhibits  varying  degrees  of  cyanosis  and 
dropsy. 

An  anxious,  distressed  expression,  watery  eyes,  with  puffy  lower 
lids,  pale  or  bluish  lips,  cheeks  and  nose  studded  with  congested 
capillaries,  cold  and  livid  extremities,  often  more  or  less  oedema- 
tous,  and  an  attitude  suggestive  of  difficulty  in  breathing,  constitute, 
severally  or  collectively,  the  appearances  observed  from  time  to  time 
in  the  different  stages  of  dilatation  of  the  heart.  It  is  by  attention 
to  details  of  this  kind  that  the  diagnosis  of  the  patient's  ailment  can 
often  be  made,  without  the  help  afforded  by  further  examination. 


DISEASES   OF   THE   MYOCARDIUM        271 

Pulse 

The  characters  of  the  pulse  in  dilatation  of  the  left  ventricle  vary 
not  only  with  the  cause  of  the  condition,  but  also  with  the  degree 
of  its  development. 

With  these  qualifications,  it  may  be  stated  generally  that  the 
pulse  of  dilatation  is  usually  rapid  and  irregular,  both  in  force  and 
frequency ;  and  if  not,  that  it  tends  to  become  so  on  slight  provoca- 
tion. The  artery,  which  may  be  large  or  small,  cannot  be  felt 
between  the  beats,  except  in  cases  of  antecedent  high  arterial 
tension,  and  in  this  event  the  vessel,  though  palpable  between  the 
beats,  is  easily  compressible.  The  pulse  wave  is  sudden,  short,  and 
badly  sustained,  and  is  easily  obliterated  by  gentle  pressure  with 
the  finger. 

Heart 

Inspection. — There  may  be  bulging  or  retraction  of  the  inter- 
costal spaces  over  some  portion  of  the  prgecordial  area.  The  apex 
beat,  when  visible,  js  seen  to  be  displaced  outwards  and  downwards. 
The  impulse  of  the  left  ventricle  is  usually  indefinite  and  diffused 
over  a  larger  area  than  in  health,  or  it  may  be  altogether  imper- 
ceptible. Pulsation  in  the  epigastrium  and  over  the  right  ventricle 
is  frequently  observed. 

Palpation. — The  localization  of  the  apex  beat  should  be 
attempted  by  means  of  the  finger,  but  it  is  often  impossible  to 
exactly  define  its  position  owing  to  the  weakness  of  the  ventricular 
contraction.  The  impulse  of  the  ventricle  is  either  uncertain, 
feeble,  and  tapping  in  character,  or  it  may  be  felt  as  a  vague  diffuse 
vibration  spread  over  a  considerable  area.  In  some  instances  the 
ventricular  impulse  is  not  perceptible,  even  on  careful  palpation, 
and  provided  this  is  not  due  to  overlapping  of  the  heart  by  lung,  it 
is  an  indication  of  great  enfeeblement  of  the  cardiac  walls. 

An  enlarged  right  ventricle  may  usurp  the  place  of  the  left,  and 
in  this  way  it  sometimes  happens  that  the  site  of  maximum  in- 
tensity of  the  cardiac  impulse  to  the  left  of  the  sternum  corre- 
sponds with  some  portion  of  the  wall  of  the  former  chamber 
instead  of  the  latter. 

Forcible  epigastric  pulsation  would  point  to  hypertrophy  of  the 
right  ventricle,  whereas  a  feeble  vibratory  impulse  in  this  situation 
would  indicate  dilatation  of  the  right  side  of  the  heart. 

Percussion. — The  area  of  cardiac  dulness  is  increased,  chiefly  in 
the  direction  of  the  left  axilla,  but  also  downwards.  The  left  limit 
of  percussion  dulness  may  extend  outwards  as  far  as  the  miid-axillary 
line.  Downwards  it  sometimes  reaches  as  low  as  the  seventh  or 
eighth  interspace.  Extension  of  the  right  limit  of  cardiac  dulness, 
if  observed,  is  due  to  concomitant  enlargement  of  the  right  side  of 
the  heart. 


272  DISEASES   OF   THE   HEART 

Auscultation. — The  first  sound  at  the  apex  is  short,  sharp,  and 
louder  than  normal,  which  is  due,  no  doubt,  to  the  absence,  in  a 
greater  or  less  degree,  of  its  muscular  element.  If  the  dilatation 
of  the  ventricle  has  given  rise  to  mitral  incompetence,  the  first 
sound  may  be  masked  by  a  systolic  murmur.  The  second  sound 
at  the  apex  is  usually  weak.  At  the  base  over  the  aortic  cartilage 
both  sounds  of  the  heart  will  be  audible,  and  it  is  sometimes 
difficult  to  distinguish  between  them,  since  the  character  of  the 
first  sound  in  dilatation  closely  resembles  that  of  the  second.  The 
second  sound  in  this  situation  tends  to  become  weaker  with  the  in- 
creasing enfeeblement  of  the  muscular  power  of  the  ventricle,  hence 
a  comparison  of  the  relative  intensity  of  the  two  sounds  may  become 
a  point  of  diagnostic  and  prognostic  value.  The  pulmonary  second 
sound  is  accentuated,  provided  the  right  ventricle  has  not  undergone 
dilatation  from  failure. 

Important  information  with  regard  to  the  vigour  of  the  ventricular 
walls  may  be  obtained  by  a  careful  observation  of  the  interval 
between  the  first  and  second  sounds  of  the  heart.  Thus  the 
interval  may  be  prolonged  until  the  sounds  become  equidistant, 
or  it  may  be  shortened,  so  that  the  second  sound  follows  the  first 
almost  immediately. 

Prolongation  of  the  interval,  or  spacing  of  the  sounds,  as  it  is 
called,  signifies  that  the  systole  of  the  ventricle  is  lengthened  in 
consequence  of  the  difficulty  experienced  by  the  chamber  in  the 
discharge  of  its  contents,  and  demonstrates  that  the  ventricle,  though 
hampered  by  the  increased  demands  upon  it,  is  attempting  success- 
fully to  complete  its  contraction. 

Approximation  of  the  sounds,  under  the  circumstances,  now  being 
considered,  means  that  the  contractile  energy  of  the  ventricular 
walls  becomes  exhausted  before  the  completion  of  the  systole.  So 
soon  as  the  pressure  in  the  aorta  exceeds  that  in  the  ventricle,  an 
event  determined  by  the  relative  degree  of  inadequacy  of  the  cardiac 
walls,  the  semilunar  valves  close,  and  the  second  sound  occurs. 

It  will  be  obvious  that  approximation  of  the  sounds  is  of  much 
graver  significance  than  prolongation  of  the  interval  between  them. 

The  phenomena  just  described  are  most  commonly  observed  in 
cases  of  continued  high  arterial  tension,  the  result  of  acute  or 
chronic  Bright's  disease. 


HYPERTROPHY  OF  THE   RIGHT  VENTRICLE 

Physiognomy 

The  aspect  presented  by  the  patient  is  that  of  the  condition 
which  has  given  rise  to  the  hypertrophy  of  the  right  ventricle. 
Since,  however,  all  the  causes  of  right-sided  hypertrophy  of  the 
heart  tend  to  interfere  with  the  pulmonary  circulation,  the  appearance 
of  the  patient  is  frequently  suggestive  of  mal-aeration  of  the  blood. 


DISEASES   OF   THE   MYOCARDIUM         273 

Pulse 

Hypertrophy  of  the  right  ventricle  exercises  no  direct  influence 
upon  the  radial  pulse.  The  modifications  in  the  character  of  the 
pulse  that  may  be  observed  are  due  not  to  the  hypertrophy  of 
the  ventrifcle,  but  to  the  accompanying  obstruction  to  the  blood 
current  in  the  pulmonary  circulation. 

One  effect  of  this  is  to  diminish  the  supply  of  blood  to  the  left 
ventricle,  and  hence  to  the  aorta  and  peripheral  vessels  ;  another 
is  to  produce  general  contraction  of  the  systemic  arterioles,  in 
consequence  of  the  stimulation  of  the  vaso-motor  centre  by  the 
imperfectly  oxygenated  blood. 

The  radial  artery,  therefore,  in  cases  of  hypertrophy  of  the  right 
ventricle,  is  small,  and  though  palpable  between  the  beats  is  easily 
compressible.  The  pulse  may  or  may  not  be  regular  in  force  and 
frequency,  while  the  wave  is  small  and  frequently  short. 

Heart 

Inspection. — The  epigastric  region  is  sometimes  prominent,  and 
there  may  be  bulging  of  the  ensiform  cartilage  and  of  the  lower  left 
costal  cartilages  at  their  junction  with  the  sternum. 

Pulsation  is  often  observed  in  the  epigastrium,  or  between  the 
lower  part  of  the  left  sternal  edge  and  the  apex  beat. 

The  jugular  veins  may  be  distended,  and  if  the  tricuspid  valve 
is  incompetent  may  show  pulsation.  The  apex  beat  is  seen  to  be 
displaced  to  the  left. 

Palpation. — The  hand  placed  in  the  epigastrium  or  over  the 
right  ventricle  experiences  the  sensation  of  a  forcible  push  or 
thrust. 

Hepatic  pulsation  may  be  due  to  the  impulse  of  the  right 
ventricle  transmitted  through  the  diaphragm,  or  to  regurgitation 
of  blood  into  the  portal  veins,  consequent  on  tricuspid  incom- 
petence. 

Percussion. — The  area  of  cardiac  dulness  is  increased  chiefly  in 
the  transverse  direction,  but  also  to  some  extent  downwards.  To 
the  right  it  may  extend  an  inch  or  more  beyond  the  right  sternal 
edge. 

Auscultation. — The  first  sound  over  the  right  ventricle  is  duller 
and  louder  than  in  health,  so  that  it  approaches  in  character  the 
normal  left  ventricle  first  sound.  If  the  tricuspid  valve  is  incom- 
petent, the  first  sound  is  accompanied,  and  more  or  less  masked, 
by  a  systolic  murmur. 

At  the  base,  over  the  pulmonary  cartilage,  the  second  sound  is 
accentuated,  so  long  as  the  tricuspid  valve  remains  competent,  and 
in  the  absence  of  valvular  disease  at  the  pulmonic  orifice.     The 
aortic  second  sound  is  usually  weak. 
T 


274  DISEASES   OF   THE    HEART 

Reduplication  of  the  first  or  second  sound  of  the  heart  is  not 
infrequently  observed  in  cases  of  hypertrophy  of  the  right  ventricle. 
The  interval  between  the  two  sounds  should  in  all  cases  be  carefully 
noted,  for  the  reasons  already  given. 


DILATATION    OF    THE    RIGHT    VENTRICLE 
Physiognomy 

The  patient  usually  presents  in  a  greater  or  less  degree  the  signs 
of  cyanosis  and  dropsy. 

Pulse 

The  pulse,  though  not  directly  affected  by  dilatation  of  the  right 
ventricle,  is  greatly  influenced  by  the  associated  lesions  in  the  lungs 
or  on  the  left  side  of  the  heart. 

As  a  rule,  therefore,  the  pulse  is  rapid,  and  irregular  both  in  force 
and  frequency.  The  artery  is  usually  small,  and  when  palpable 
between  the  beats  is  easily  compressible. 

The  pulse  wave  is  small,  short,  and  weak. 

Heart 

Inspection. — There  may  be  bulging  of  the  lower  part  of  the 
sternum,  and  of  the  immediately  adjacent  costal  cartilages. 

The  epigastrium  is  usually  prominent  and  not  infrequently  shows 
pulsation. 

The  impulse  of  the  right  ventricle  is  diffused  over  the  portion 
of  the  prgecordial  area  between  the  apex  beat  and  left  sternal  edge 
as  high  as  the  second  interspace.  Pulsation  to  the  right  of  the 
sternum  in  the  second  and  third  interspaces  may  be  due  to  an 
enlarged  right  auricle. 

The  veins  in  the  neck  appear  distended,  and  there  may  be  jugular 
and  hepatic  pulsation. 

Palpation. — The  impulse  of  the  right  ventricle  felt  over  the  lower 
portion  of  the  sternum  and  in  the  epigastrium  is  feeble,  tapping, 
and  diffused,  or  it  may  be  quite  imperceptible.  The  jugular  veins 
may  fill  from  below,  when  emptied  by  pressure  with  the  finger  from 
below  upwards,  in  consequence  of  regurgitation  of  blood  through 
the  tricuspid  opening.  A  similar  cause  can  give  rise  to  pulsation 
of  the  liver,  which  is  sometimes  observed. 

Percussion. — The  area  of  cardiac  dulness  is  increased  chiefly  in 
the  lateral  direction,  and  may  extend  an  inch  or  more  to  the  right 
of  the  sternum. 

Auscultation. — The  first  sound  over  the  right  ventricle  is  short 
and  sharp,  and  it  may  be  accompanied  by  a  systolic  murmur,  which 


DISEASES   OF   THE   MYOCARDIUM         275 

is    most   distinctly   heard   over   the    ensiform   cartilage   and   lower 
portion  of  the  sternum. 

The  pulmonary  second  sound  loses  its  accentuation  with  the 
occurrence  of  tricuspid  incompetence.  The  aortic  second  sound 
is  usually  weak. 


HYPERTROPHY  AND    DILATATION  OF  THE   LEFT 
AURICLE 

Since  hypertrophy  of  the  left  auricle  is  almost  invariably  found 
in  association  with  dilatation  of  its  cavity,  it  will  be  convenient 
and  sufficiently  accurate  to  consider  the  physical  signs  of  enlarge- 
ment of  the  chamber,  irrespective  of  its  exact  mode  of  causation. 

A  similar  plan  will  be  followed  in  the  case  of  the  right  auricle. 

It  may  be  pointed  out,  however,  that  as  a  rule  dilatation  pre- 
ponderates over  hypertrophy  in  all  forms  of  auricular  enlargement. 
It  is  stated  that  pulsation  in  the  third  left  interspace,  due  to  the 
systole  of  an  enlarged  left  auricle,  may  sometimes  be  observed  in 
the  case  of  children  and  of  persons  with  thin  chest  walls.  Dulness 
in  the  second  and  third  left  intercostal  spaces  close  to  the  sternum 
has  been  ascribed  to  enlargement  of  the  left  auricle,  but  this  is 
not  admitted  by  all  observers. 


HYPERTROPHY  AND   DILATATION  OF  THE  RIGHT 
AURICLE 

Enlargement  of  the  right  auricle  gives  rise  to  dulness  in  the 
second,  third,  and  fourth  intercostal  spaces,  extending  for  an  inch 
or  more  to  the  right  of  the  sternal  edge.  Pulsation  may  be  caused 
in  this  situation  by  the  systole  of  an  enlarged  auricle. 

In  some  cases  of  tricuspid  obstruction  the  hypertrophy  of  the 
auricle  may  be  sufficient  to  give  rise  to  a  backflow  of  blood  into 
the  veins  during  the  systole  of  the  chamber. 

In  such  an  event  the  venous  pulsation  would,  of  course,  be  pre- 
systolic as  regards  its  relation  to  the  cardiac  cycle. 


DIAGNOSIS 

The  first  step  in  the  diagnosis  is  the  exclusion  of  the  conditions 
which  may  simulate  or  mask  enlargement  of  the  heart.  If,  in  this 
way,  the  diagnosis  of  cardiac  enlargement  is  established,  three  points 
remain  to  be  considered,  viz.  (i)  whether  the  increase  in  the  size 
of  the  heart  is  due  to  hypertrophy  or  to  dilatation,  (2)  whether 
the  enlargement  of  the  organ  is  partial  or  general,  and  (3)  the 
cause  of  the  increase  in  size  of  the  heart 


276  DISEASES   OF   THE    HEART 

The  conditions  which  may  simulate  or  mask  enlargement  of  the 
heart  will  now  be  considered. 

Bulging  of  the  chest  wall  involving  the  prsecordium  may  be  due 
to  congenital  malformation,  rickets,  mediastinal  tumours,  left  pleural 
effusion,  etc. 

Attention  to  shape,  position,  and  outline  of  the  prominent  areas 
arising  from  these  causes  is  usually  sufficient  to  distinguish  them 
from  the  prsecordial  bulging  associated  with  diseases  of  the  heart 
and  pericardium. 

For  similar  reasons  the  recession  of  the  prsecordium  due  to  con- 
genital malformations,  retraction  of  the  left  lung,  and  long-continued 
pressure  in  this  situation,  as  in  the  case  of  shoemakers,  joiners,  etc., 
will  not  be  confounded  with  the  effects  of  pericardial  adhesions. 

In  a  case  of  doubt,  the  history  of  the  patient  would  be  of  great 
assistance  in  clearing  up  the  diagnosis. 

It  has  already  been  mentioned  that  the  dulness  due  to  cardiac 
enlargement  may  be  masked  by  the  overlapping  of  the  heart  by 
lung.  The  recognition  of  the  existence  of  pulmonary  emphysema 
would  suffice  to  exclude  this  source  of  error. 

Enlargement  of  the  heart  may  be  simulated  by  exposure  of  the 
organ,  consequent  on  retraction  of  the  anterior  margins  of  the 
lungs,  by  consolidation  of  the  anterior  portions  of  either  lung,  by 
local  pleural  effusion,  by  aneurism  of  the  ascending  portion  of  the 
aorta  or  by  mediastinal  tumours  above  the  base  of  the  heart,  by 
forward  displacement  of  the  organ,  and  by  pericardial  effusion. 

Except  in  the  case  of  pericardial  effusion,  the  differential  diagnosis 
is  not  usually  a  matter  of  very  great  difficult)',  and  depends  on  the 
history  of  the  patient  and  on  a  careful  estimation  of  the  extent  and 
outline  of  the  areas  of  dulness,  and  also  on  the  associated  symptoms 
and  physical  signs. 

Pericardial  effusion  may  be  distinguished  by  the  shape  of  the 
outline  of  dulness  and  its  relation  to  the  apex  beat,  by  the  position 
and  character  of  the  cardiac  impulse,  by  the  presence  of  friction 
sounds,  and  by  the  history  and  associated  conditions  (see  p.  125). 

Displacement  of  the  heart  and  apex  beat  to  the  left  due  to 
retraction  of  the  left  lung,  effusion  of  air  or  fluid  into  the  right 
pleural  cavity,  elevation  of  the  diaphragm,  and  aneurism  of  the 
ascending  aorta  may  be  confounded  with  cardiac  enlargement. 

Under  these  circumstances,  however,  the  area  of  cardiac  dulness, 
though  dislocated,  is  not  increased,  and  this  fact,  taken  in  conjunc- 
tion with  the  presence  of  a  cause  for  displacement  of  the  heart,  and 
the  absence  of  any  discoverable  cause  of  enlargement,  should  go 
a  long  way  to  remove  any  difficulty  that  may  be  experienced  in 
forming  a  correct  diagnosis. 


DISEASES    OF   THE   MYOCARDIUM         277 

The  Differential  Diagnosis  of  Hypertrophy  and  Dilatation 

Although  hypertrophy  and  dilatation  are  so  frequently  found  in 
combination,  it  is  convenient  for  clinical  purposes  to  consider  a 
heart  hypertrophied  or  dilated  according  as  one  or  other  condition 
predominates. 

In  attempting  to  decide  which  of  these  conditions  preponderates 
in  the  production  of  cardiac  enlargement,  reliance  should  be  placed 
chiefly  on  the  evidence  afforded  by  the  shape  of  the  precordial 
dulness,  and  by  the  character  of  the  impulse  and  of  the  sounds, 
together  with  the  absence  or  presence  of  the  signs  of  disturbance  of 
the  circulation. 

It  may  be  stated  generally  that  hypertrophy  or  dilatation  pre- 
dominates according  as  enlargement  of  the  heart  exists  without  or 
with  the  signs  of  circulatory  embarrassment.  — ^ 

The  Distribution  of  Hypertrophy  and  Dilatation  in 
Enlargement  of  the  Heart 

All  or  any  of  the  chambers  of  the  heart  may  be  affected  by 
hypertrophy  or  dilatation. 

The  diagnosis  of  the  general  or  partial  involvement  of  the  organ 
rests  on  the  causes  of  the  cardiac  enlargement,  considered  in  con- 
junction with  their  known  effects,  and  on  the  symptoms  and  physical 
signs  which  are  associated  with  hypertrophy  and  dilatation  of  the 
different  chambers  of  the  heart. 

The  Cause  of  the  Cardiac  Enlargement  ^ 

The  importance  that  attaches  to  the  elucidation  of  the  cause  of 
enlargement  of  the  heart  cannot  be  too  strongly  insisted  upon,  since 
it  is  on  this  point  that  the  prognosis  and  treatment  largely  turn. 

In  those  instances  in  which  cardiac  enlargement  is  due  to  disease 
of  the  heart,  lungs,  or  kidneys,  the  cause  is  as  a  rule  easily 
recognized. 

It  is  in  the  diagnosis  of  the  source  of  dilatation  from  failure  that 
difficulty  most  commonly  arises.  Here  not  only  must  primary 
dilatation  of  the  heart  be  distinguished  from  dilatation  secondary  to 
valvular  or  pericardial  disease,  etc.,  but  the  precise  cause  of  the 
failure  of  the  muscular  walls,  in  any  event,  must  if  possible  be 
determined.  ~ 

The  difficulties  that  may  attend  this  part  of  the  diagnosis  can  be 
most  conveniently  illustrated  by  the  study  of  a  concrete  example. 

Displacement  of  the  apex  beat  to  the  left,  with  a  corresponding 
extension  of  the  left  limit  of  cardiac  dulness  and  an  apical  systolic 
murmur,  are  the  physical  signs  associated  with  regurgitation  through 
the  mitral  opening,  due  to  valvular  disease  or  to  muscular  in- 
competence, consequent  on  primary  dilatation  of  the  left  ventricle. 


278  DISEASES   OF   THE   HEART 

The  differential  diagnosis  is  a  matter  of  great  importance  on 
account  of  its  bearing  on  the  prognosis,  which  is  very  different 
in  the  two  conditions,  since  the  one  is  permanent  and  irremediable, 
whereas  the  other  is  often  temporary  and  curable. 

The  character  and  extent  of  propagation  of  the  murmur,  with  its 
relation  to  the  first  sound,  the  character  of  the  pulse,  the  causal 
indications,  and  the  effects  of  treatment  are  the  points  which  afford 
the  most  reliable  means  of  distinction. 

Thus  a  loud,  well-conducted  murmur,  partially  or  wholly  obscuring 
the  first  sound;  a  small,  weak,  irregular  pulse;  a  definite  history 
of  rheumatic  fever ;  and  an  increase  in  the  intensity  of  the  murmur 
under  treatment,  would  point  to  valvular  incompetence. 

On  the  other  hand,  a  clear,  short,  and  sharp  first  sound,  followed 
and  not  obscured  by  the  murmur,  which  is  not  well  conducted 
towards  the  left  axilla;  a  pulse  of  variable  character,  but  possibly 
exhibiting  increased  tension;  the  presence  of  ana2mia,  or  other  cause 
of  malnutrition ;  and  the  disappearance  of  the  murmur  under  treat- 
ment, would  indicate  muscular  incompetence. 

In  either  event  the  exact  cause  of  the  dilatation  from  failure 
should  be  diligently  sought  for. 

It  may  depend  on  the  operation  or  co-operation  of  many  forces, 
chief  among  which  are  mental  or  bodily  over-exertion,  excitement, 
anxiety,  exposure,  chill,  dyspepsia,  ansemia,  or  malnutrition  from 
other  causes,  and  pulmonary  or  other  complications.  Indiscretions 
in  eating  and  drinking,  sexual  excess,  neglect  of  the  action  of  the 
bowels,  the  abuse  of  alcohol,  tea,  tobacco,  contribute  towards  the 
same  result. 

PROGNOSIS 

The  attempt  to  forecast  the  course  and  issue  of  affections  of  the 
myocardium  is  no  whit  less  important  than  in  the  case  of  valvular 
disease  of  the  heart. 

The  problem  in  myocardial  lesions  is,  however,  rendered  more 
complicated  by  the  fact  that  no  such  correlation  exists  between  the 
extent  of  the  disease  and  its  effects  on  the  heart  and  circulation 
as  obtains  in  valvular  affections. 

In  the  absence  of  this  important  source  of  knowledge,  the 
prognosis  in  myocardial  disease  turns  on  collateral  considerations 
of  cause  and  effect,  which,  though  productive  of  valuable  evidence, 
lack  the  exactitude  and  precision  essential  to  the  formation  of  a 
reliable  forecast  of  the  probable  course  of  events. 

However,  in  spite  of  these  difficulties,  it  is  frequently  possible, 
by  means  of  a  careful  and  complete  survey  of  all  the  phenomena 
associated  with  lesions  of  the  cardiac  walls,  to  arrive  at  a  fairly 
accurate  estimate  of  their  course  and  duration. 

The  subject  will  be  considered  under  the  heads  of  hypertrophy 
and  dilatation  respectively. 


DISEASES   OF   THE   MYOCARDIUM         279 

Hypertrophy 

Provided  that  compensation  is  efficient,  and  also  that  the  con- 
ditions, both  local  and  general,  are  favourable  for  the  maintenance 
of  hypertrophy,  the  prognosis  is  favourable. 

In  estimating  the  probable  duration  of  compensation,  the  age,  sex, 
occupation,  and  condition  in  life  of  the  patient  must  be  taken  into 
account,  as  well  as  the  nature  and  tendency  of  the  morbid  change 
which  has  given  rise  to  the  hypertrophy. 

It  sometimes,  though  rarely,  happens  that  the  cause  of  the  hyper- 
trophy is  partially  or  wholly  removable,  and,  other  things  being 
equal,  the  outlook  is  propitious  in  proportion  to  the  degree  of  this 
possibility. 

As  a  rule,  however,  the  cause  is  abiding,  and  furthermore,  it  may 
be  either  stationary  or  progressive. 

The  prognosis,  speaking  generally,  is  more  favourable  in  the 
event  of  the  first  alternative  than  in  that  of  the  second. 

It  must  be  borne  in  mind  that,  in  cases  of  cardiac  hypertrophy 
due  to  high  arterial  tension,  the  rupture  of  a  vessel  in  the  brain  or 
elsewhere  may  upset  an  otherwise  favourable  prognosis. 

Dilatation  from  Failure 

In  attempting  to  forecast  the  issue  of  dilatation  of  the  heart  from 
failure,  it  is  necessary  to  carefully  weigh  and  compare  the  indications 
derived  from  the  following  sources  of  information  : — - 

1.  The  general  state  of  the  patient. 

2.  The    condition    of    the    cardiac    muscle   as    shown    by   the 

symptoms  and  physical  signs. 

3.  The  cause  of  the  failure  of  the  cardiac  walls. 

4.  The  history,  habits,  etc.,  of  the  patient. 

5.  The  presence  or  absence  of  complications. 

6.  The  effects  of  treatment. 

Each  of  these  factors  in  the  prognosis  will  now  be  considered 
in  detail. 

I.  The  general  state  of  tlie  patient. — The  severity  of  the 
symptoms  corresponds  with  the  degree  of  disturbance  of  the 
circulation,  and  hence  with  the  extent  to  which  the  propulsive 
power  of  the  heart  is  impaired. 

Indications  of  impending  danger  may  appear  on  the  venous 
or  on  the  arterial  side  of  the  circulation,  and  among  the  signs 
and  symptoms  of  serious  import  may  be  mentioned  extensive  water- 
logging of  the  tissues,  severe  and  protracted  vomiting,  continued 
sleeplessness,  great  bodily  weakness,  and  attacks  of  faintness  or 
extreme  breathlessness. 


28o  DISEASES    OF   THE    HEART 

2.  The  condition  of  the  cardiac  muscle  as  shown  by  tho 
symptoms  and  physical  signs. — The  estimate  so  far  made  of  the 
degree  of  efficiency  of  the  cardiac  muscle  must  be  supplemented 
by  an  examination  of  the  pulse  and  heart.  Extreme  irregularity 
of  the  pulse,  or  a  great  increase  in  frequency,  if  long  continued, 
is  of  bad  omen. 

Disappearance  of  previously  existing  high  arterial  tension,  not 
due  to  treatment,  implies  failure  of  the  muscular  power  of  the 
heart,  and  is  therefore  an  unfavourable  sign. 

The  degree  of  cardiac  vigour  is  gauged  more  accurately  by  the 
strength  of  the  impulse  and  by  the  extent  of  the  percussion 
dulness,  together  with  the  character  and  time  relations  of  the 
sounds  of  the  heart. 

A  feeble,  hesitating  impulse,  great  increase  in  the  lateral  extent 
of  dulness,  and  approximation  or  weakness  of  the  sounds,  are 
indicative  of  serious  enfeeblement  of  the  cardiac  walls,  and  warrant 
therefore  a  serious  prognosis. 

On  the  other  hand,  a  fair  strength  of  impulse,  with  some  accen- 
tuation or  spacing  of  the  sounds,  implies  a  certain  degree  of  cardiac 
vigour,  and  consequently  renders  the  outlook  more  hopeful. 

3.  The  cause  of  the  failure  of  the  cardiac  walls. — If  the  cause 

of  failure  can  be  discovered  and  removed  the  prognosis  will  be 
favourable.  Thus  the  effects  of  over-exertion,  ansemia,  or  mal- 
nutrition, dyspepsia,  etc.,  may  be  remedied  by  suitable  treatment, 
and  in  this  way  the  muscular  power  of  the  heart  may  be  restored 
and  the  normal  balance  of  the  circulation  re-established. 

On  the  other  hand,  if  the  enfeeblement  of  the  cardiac  walls 
proceeds  from  irremovable  causes,  as,  for  instance,  acute  inter- 
current disease  or  radical  weakness  of  the  heart,  the  outlook  will 
be  most  discouraging. 

4.  The  history  and  habits  of  the  patient. — The  age,  history, 
and  habits  of  the  patient  exercise  an  important  influence  on  the 
course  of  the  disease.  Youth,  a  good  family  history,  a  regular 
mode  of  life,  and  abstemious  habits  will  tell  in  favour  of  recovery. 
On  the  other  hand,  a  constitution  lacking  hereditary  vigour,  and 
undermined  by  exposure,  the  abuse  of  alcohol,  etc.,  would  offer  but 
a  small  margin  of  recuperative  power. 

5.  The  presence  or  absence  of  complications.  —  Concurrent 
disease  of  the  kidneys,  lungs,  or  liver  would  detract  greatly  from 
the  prospects  of  recovery,  not  only  by  reason  of  the  increased 
strain  which  is  thrown  on  the  heart,  but  also  on  account  of  the 
general  interference  with  nutrition  and  metabolism,  due  to  functional 
derangement  of  these  organs. 

The  absence  of  complications  is  of  favourable  import. 

6.  The  effects  of  treatment.— The  manner  in  which  the  heart 
responds  to  treatment  affords  an  important  indication  of  the  con- 


DISEASES   OF   THE   MYOCARDIUM         281 

di("ion  of  the  cardiac  muscle.  A  well-marked  and  rapidly  produced 
beneficial  effect  implies  that  the  walls  of  the  organ  are  still  sound, 
whereas  the  absence  of  any  response  to  treatment  is  significant  of 
serious  deterioration  of  the  muscular  tissue  of  the  heart. 


TREATMENT 
Hypertrophy 

In  a  previous  section  it  was  pointed  out  that  hypertrophy  of  the 
heart,  although  it  may  be  efficient  or  inefficient,  never  exceeds  the 
requirements  of  the  occasion  which  has  given  rise  to  it.  Per  se, 
therefore,  hypertrophy  does  not  call  for  treatment,  but  rather  sug- 
gests it.  Hypertrophy  is  the  natural  method  of  combating  disease, 
and,  as  such,  should  be  sedulously  encouraged  and  maintained. 

The  treatment  indicated  by  hypertrophy  consists,  then,  in  the 
promotion  and  preservation  of  the  integrity  of  the  cardiac  muscle 
fibre  and  in  the  removal  or  modification,  so  far  as  possible,  of  the 
causes  which  have  given  rise  to  the  increase  in  the  size  of  the  heart. 

The  conditions  which  conduce  to  the  furtherance  of  the  first 
object  may  be  summed  up  under  the  heads  of  hygienic,  dietetic,  and 
medicinal  treatment,  and  will  now  be  briefly  considered. 

Hygienic  treatment. — The  mode  of  life  and  habits  of  the  patient 
should  be  regulated  with  the  view  of  promoting  the  general  health 
and  of  avoiding,  to  the  greatest  possible  extent,  the  causes  of  cardiac 
strain  and  excitement. 

The  action  of  the  skin,  kidneys,  and  bowels  must  be  carefully 
attended  to  and  occasionally  assisted  by  suitable  therapeutic  means. 

Chill  should  be  guarded  against  by  the  use  of  woollen  under- 
clothing, and  the  incidence  of  acute  disease,  so  far  as  possible, 
prevented. 

Acute  intercurrent  affections,  more  especially  rheumatism  and 
pulmonary  disorders,  should  be  vigorously  treated,  the  heart  mean- 
while being  carefully  watched  for  any  indications  of  failure,  which, 
when  observed,  should  be  met  by  the  exhibition  of  stimulants  and 
cardiac  tonics. 

The  patient  should  be  surrounded  by  wholesome  nervous  in- 
fluences and  removed  so  far  as  practicable  from  all  sources  of 
mental  worry  and  excitement. 

While  a  moderate  amount  of  exercise  is  beneficial,  over-exertion  in 
any  form  must  be  rigidly  eschewed. 

It  is  by  the  intelligent  application  of  hygienic  measures  of  this 
kind  that  tranquillity  of  the  circulation  is  promoted  and  the  strain 
on  the  heart  reduced  to  the  lowest  possible  limits. 

Dietetic  treatment. — The  diet  should  be  nutritious,  non-stimulat- 
ing, and  easily  digestible,  and  ought  to  contain  an  ample  proportion 


282  DISEASES   OF  THE    HEART 

of  nitrogenous  food.  Alcohol  may  be  taken  sparingly,  and  at  meal 
times  only.  Over-eating  and  drinking  must  be  scrupulously  avoided. 
Errors  of  digestion  should  be  corrected  without  delay,  for  not 
only  does  dyspepsia  do  harm  by  interfering  with  nutrition,  but  by 
giving  rise  to  flatulence  it  directly  embarrasses  the  heart's  action. 

Medicinal  treatment. — One  of  the  chief  desiderata  in  cases  of 
cardiac  hypertrophy  is  an  adequate  supply  of  healthy  blood  to  the 
myocardium.  If  this  object  is  not  achieved  by  the  measures  already 
indicated,  it  must  be  promoted  by  medicinal  means.  The  drugs 
most  useful  for  the  purpose  are  iron  and  arsenic,  which  may  be 
administered  either  separately  or  in  combination  with  one  another, 
or  with  some  cardiac  tonic  such  as  digitalis  or  strophanthus.  During 
the  use  of  these  remedies  the  digestive  organs  should  be  attended 
to  and  the  bowels  kept  open  by  mild  saline  and  aloetic  aperients. 

Excited  action  of  the  heart  may  be  controlled  by  the  appHcation 
of  cold  or  a  belladonna  plaster  to  the  prsecordium,  and  the  internal 
administration  of  dilute  hydrocyanic  acid,  belladonna,  bromide  of 
ammonium,  or  small  doses  of  opium.  The  use  of  cardiac  depres- 
sants for  this  purpose  may  be  attended  with  danger,  and  should  be 
avoided. 

The  treatment  of  the  cause. — In  the  majority  of  instances, 
hypertrophy  of  the  heart  depends  upon  causes  which  are  organic, 
permanent,  and  irremovable.  Under  such  circumstances  the  treat- 
ment already  indicated  will  do  much  to  diminish  the  strain  upon 
the  heart  and  to  encourage  and  maintain  the  existing  hypertrophy 
of  the  organ.  Beyond  this  little  or  nothing  can  be  effected  by 
therapeutic  means. 

In  those  cases,  however,  in  which  hypertrophy  of  the  heart  is  due 
to  prolonged  muscular  effort  or  high  arterial  tension  a  much  greater 
opportunity  is  afforded  for  treatment. 

In  the  first  event,  the  removal  of  the  cause  and  the  substitution 
of  complete  rest  will  usually  suffice  for  the  disappearance  of  the 
hypertrophy. 

Again,  high  arterial  tension  may  be  removed,  diminished,  or  con- 
trolled with  a  corresponding  degree  of  benefit  to  the  condition  of 
the  heart. 

Since  high  tension  in  the  arterial  system  is  due  for  the  most  part 
to  the  presence  in  the  blood  of  imperfectly  oxidised  nitrogenous 
waste  products,  the  aim  of  treatment  is  to  remove  these  impurities 
and  prevent  their  re-formation. 

To  this  end  fresh  air  and  regular  exercise  in  one  form  or  another 
are  essential. 

The  diet  must  be  regulated  with  the  object  of  restricting  the 
amount  of  nitrogenous  food,  which,  in  the  shape  of  the  flesh  of 
beast  or  bird,  should  not  be  taken  more  often  than  once  a  day. 
Strict  moderation  must  also  be  observed  with  respect  to  the  use 
of  alcoholic  beverages. 


DISEASES   OF   THE    MYOCARDIUM         283 

In  those  instances  in  which  plethora  is  a  factor  in  the  production 
of  high  arterial  tension,  it  may  become  necessary  to  limit  the  amount 
of  fluid  taken  at  meals. 

The  medicinal  means  by  which  the  products  of  imperfect  nitro- 
genous metabolism  are  got  rid  of,  and  the  resistance  to  the  onward 
flow  of  blood  through  the  small  arteries  and  capillaries  is  diminished, 
consist  in  the  administration  of  purgatives  and  other  eliminants. 

The  most  useful  drug  for  this  purpose  is  mercury,  preferably  in 
the  form  of  calomel,  blue  pill,  or  grey  powder,  which  may  be  given 
in  doses  of  two  or  three  grains,  once  or  twice  a  week,  in  combina- 
tion with  a  course  of  mild  saline  aperients,  such  as  the  phosphate  or 
sulphate  of  soda. 

The  salts  of  sodium,  lithium,  and  potassium,  more  particularly 
the  latter,  have  valuable  eliminative  properties,  and  may  be  pre- 
scribed, from  time  to  time,  in  conjunction  with  the  above-mentioned 
remedies. 

The  reduction  of  peripheral  tension  may  also  be  effected  by  the 
direct  abstraction  of  blood,  or  by  the  administration  of  nitro- 
glycerine, erythrol  tetranitrate,  and  the  nitrites,  which  act  by  pro- 
ducing relaxation  of  the  muscular  coats  of  the  arterioles. 

Dilatation  from  Failure 

The  treatment  of  dilatation  of  the  heart  from  failure  may  be 
approached  in  one  of  two  ways,  i.e.  from  the  side  of  the  cause  or 
of  the  effects  of  the  morbid  process. 

Either  procedure  has  its  advantages,  but,  speaking  generally,  the 
first  method  is  better  suited  to  the  slighter  degrees  of  dilatation, 
while  the  second  is  more  adapted  to  the  advanced  stages  of  the 
affection.  The  reason  for  this  is,  that  in  the  one  case  the  treatment 
of  the  cause  is  usually  sufficient  to  undo  and  remove  the  effects  of 
the  lesion,  whereas  in  the  other  it  is  not.  Moreover,  the  urgency 
of  the  symptoms  in  advanced  dilatation  do  not  admit  of  the  delay 
which  the  discovery  and  treatment  of  the  cause  often  entail. 

Nevertheless,  in  many  instances  it  is  possible  to  treat  both  the 
cause  and  effects  of  dilatation  simultaneously,  and  where  this  is 
feasible  it  should  be  done.  If,  however,  the  cause  of  the  morbid 
process  cannot  be  discovered,  or  is  irremediable,  treatment  must  of 
necessity  be  directed  towards  the  effects. 

The  treatment  of  dilatation  of  the  heart  from  failure  will  there- 
fore be  considered  under  the  heads  of  "  Cause  "  and  "  Effects,"  and 
this  division  of  the  subject  is  not  only  convenient  for  descriptive 
purposes,  but  also  offers  many  practical  advantages,  not  the  least 
being  that  it  forms  the  basis  of  rational  therapeutics. 

Treatment  of  the  cause. — Dilatation  of  the  heart  from  failure 
may  be  due  to  increased  intra-cardiac  pressure,  consequent  on 
organic  valvular  disease  or  high  arterial  tension,  or  it  may  depend 


284  DISEASES   OF   THE    HEART 

on  impairment  of  the  muscular  power  of  the  heart,  the  result  of 
overstrain,  malnutrition,  or  of  structural  changes  in  its  walls. 

The  cause,  in  the  case  of  organic  valvular  disease,  is  permanent 
and  irremediable,  and  requires,  therefore,  no  further  consideration. 

The  important  influence  exerted  by  high  arterial  tension  in  the 
production  of  dilatation  of  the  heart  has  already  been  insisted  on, 
and  the  treatment  of  this  cause  of  cardiac  enlargement  will  be  found 
under  the  head  of  hypertrophy  of  the  organ. 

The  dilatation  of  the  heart  associated  with  exposure,  unhealthy 
hygienic  surroundings,  insufficient  or  bad  feeding,  etc.,  is  usually 
found  among  the  poorer  classes,  and,  as  a  rule,  can  be  easily  cured 
by  the  rest,  warmth,  and  wholesome  diet  which  is  to  be  obtained  in 
a  hospital. 

The  treatment  may,  if  necessary,  be  supplemented  by  the  ad- 
ministration of  tonics  of  various  kinds,  among  which  iron  is  usually 
the  most  suitable,  given  in  combination  with  arsenic,  strychnine,  or 
phosphorus. 

Cardiac  tonics  are  seldom  required,  and  in  the  absence  of  some 
special  indication  need  not  be  prescribed. 

A  similar  mode  of  treatment  is  applicable  to  those  cases  of 
dilatation  of  the  heart  which  are  dependent  on  anaemia,  either 
simple  or  pernicious. 

Malnutrition  of  the  heart  in  common  with  the  rest  of  the  organs 
of  the  body  is  due  to  a  variety  of  other  causes,  as,  for  instance, 
over-feeding,  insufficient  exercise,  intemperance  in  the  use  of  alcohol 
and  tobacco,  sexual  excesses,  and  the  like. 

The  cardiac  dilatation  which  may  be  observed  under  such  con- 
ditions is  curable  only  when  the  patient  is  ready  and  able  to  give 
up  his  indulgences,  and  is  prepared  to  regulate  his  habits  and 
mode  of  life  in  accordance,  so  far  as  practicable,  with  the  dictates 
of  health. 

A  plain  and  spare  diet  should  be  ordered,  and  the  bowels  must  be 
kept  freely  open  by  means  of  saline  aperients  and  the  occasional 
use  of  a  brisk  mercurial  purge. 

Hsematinics  are  frequently  of  service,  and  they  may  be  advanta- 
geously combined  with  digitalis,  or  with  other  cardiac  and  general 
tonics. 

It  is  sometimes  advisable  to  preface  exercise  by  a  few  weeks  com- 
plete rest  in  bed,  during  which  time  tissue  change  may  be  promoted 
and  nutrition  improved  by  the  assistance  of  massage  and  passive 
movements  of  the  limbs. 

Exercise  must  be  cautiously  and  gradually  resumed,  and  at  first 
may  take  the  form  of  easy  walking  on  level  ground.  Later  the 
amount  of  exercise  must  be  regulated  by  the  requirements  of  each 
individual  case. 

It  may  be  laid  down,  as  a  general  rule,  that  any  exercise  which 
does  not  give  rise  to  shortness  of  breath  may  be  indulged  in  with 
safety  and  benefit. 


DISEASES   OF   THE   MYOCARDIUM        285 

A  brief  reference  must  be  made  to  one  or  two  of  the  special 
methods  employed  in  the  treatment  of  dilatation  of  the  heart  from 
failure. 

The  Schott  treatment,  which  has  of  late  years  attracted  very 
favourable  notice,  comprises  the  use  of  specially  medicated  baths, 
in  conjunction  with  a  carefully  graduated  series  of  resisted  muscular 
movements.  Although  usually  practised  together,  either  procedure 
may  be  employed  alone.  This  mode  of  treatment  appears  to  be 
applicable  to  failure  of  the  heart  from  any  cause,  but  it  is  particularly 
adapted  to  those  forms  of  dilatation  which  depend  upon  structural 
and  nutritional  lesions  of  the  myocardium.     (See  p.  240.) 

From  the  results  so  far  obtained  it  would  seem  that  the  treatment 
is  likely  to  occupy  a  permanent  and  prominent  place  in  cardiac 
therapeutics. 

Slight  degrees  of  dilatation  of  the  heart  are  sometimes  greatly 
benefited  by  the  system  of  graduated  hill  climbing  at  high  altitudes, 
devised  by  CErtel.  The  amount  of  food  and  water  that  is  taken 
is  also  carefully  regulated  and  restricted.  This  method  of  treatment 
is  open  to  the  objection  that  it  is  difficult  to  regulate  the  amount  of 
exertion  performed  by  the  patient,  and,  unless  great  care  is  observed, 
strain  is  imposed  on  the  heart,  which  may  be  productive  of  disastrous 
results. 

The  treatment  of  dilatation  of  the  heart  due  to  over-exertion 
consists  in  the  removal  of  the  cause,  and  the  observance  of  com- 
plete rest  for  some  weeks  at  least. 

Exercise  must  be  resumed  gradually  and  cautiously,  and  any  thing 
like  severe  or  sudden  exertion  must  be  carefully  avoided  for  many 
months.  ■ — 

Dilatation  of  the  heart  dependent  upon  acute  intercurrent  disease 
must  be  treated  on  the  lines  which  were  indicated  when  speaking  of 
the  maintenance  of  hypertrophy  under  similar  circumstances. 

Treatment  of  the  effects. — The  ultimate  effects  of  dilatation  of 
the  heart  from  failure  are  seen  both  on  the  arterial  and  on  the 
venous  side  of  the  circulation,  and  lead  in  the  one  case  to  anaemia, 
and  in  the  other  to  engorgement. 

Arterial  anaemia  is  the  outcome  of  the  defective  driving  power  of 
the  ventricles. 

Venous  engorgement  is  the  result  of  the  obstruction  to  the  out- 
flow of  blood  from  the  great  veins,  consequent  on  the  high  pressure 
that  obtains  in  the  right  auricle,  which  in  turn  depends  on  the 
general  increase  of  intra-cardiac  and  pulmonary  tension,  working 
backwards  through  the  tricuspid  opening  by  way  of  the  left  heart, 
lungs,  and  right  ventricle. 

The  object  of  treatment,  therefore,  is  to  increase  the  power  and 
diminish  the  work  of  the  heart,  and  at  the  same  time  to  relieve 
cardiac  distension  and  venous  engorgement,  to  alleviate  pain  and 
distress,  and  to  promote  nutrition. 

The  attempt  to  fulfil  these  indications  must  be  made  in  the  first 


286  DISEASES    OF   THE    HEART 

instance  from  the  venous  side  of  the  circulation,  since  it  is  easier, 
safer,  and  more  effective  to  reUeve  the  heart  of  its  arrears  of  work 
than  it  is  to  increase  the  force  of  its  contractions. 

The  relief  of  cardiac  distension  and  venous  engorgement,  and  of 
tlie  work  done  by  the  heart. — Venesection  affords  the  most  speedy 
and  effectual  means  of  reUeving  distension  of  the  right  heart. 

Except,  however,  in  cases  of  acute  dilatation  this  method  of  treat- 
ment is  seldom  practised,  by  reason  of  the  inability  of  the  enfeebled 
cardiac  muscle  to  respond  to  any  sudden  form  of  rehef.  All  that  is 
necessary  in  the  way  of  removal  of  blood  can,  as  a  rule,  be  more 
safely  and  conveniently  effected  by  means  of  the  appHcation  of 
eight  or  ten  leeches  over  the  prsecordial  or,  preferably,  the  hepatic 
region. 

The  relief  afforded  by  this  procedure  is  usually  very  remarkable, 
and  is,  moreover,  quickly  produced. 

At  the  same  time,  free  purgation  must  be  obtained,  with  the  object 
of  removing  or,  at  least,  of  mitigating  the  engorgement  of  the  liver 
and  portal  circulation,  and  of  diminishing  arterio-capillary  resistance, 
and  therefore  of  relie\-ing  the  work  of  the  heart. 

For  this  purpose  two  or  three  grains  of  calomel  may  be  given  in 
combination  with  thirtj'  or  forty  grains  of  compound  jalap  powder, 
which  is  by  far  the  most  useful  of  the  hydragogue  cathartics  in  cases 
of  cardiac  failure. 

The  bowels  may  be  subsequently  regulated  by  the  use  of  one  or 
two  grains  of  blue  pill,  calomel,  or  grey  powder  with  colocynth  and 
hyoscyamus,  which  can  be  taken  at  night,  once  or  twice  a  week,  and 
followed  the  next  morning  by  a  mild  saline  aperient. 

The  action  of  the  kidneys  will  be  promoted  by  these  measures, 
and,  if  necessary,  may  be  further  encouraged  by  the  administration 
of  cardio-vascular  diuretics  and  direct  renal  stimulants,  such  as 
spiritus  stheris  nitrosi,  scoparium,  and  the  Hke. 

The  salts  of  potassium  are  particularly  useful  as  diuretics,  on 
account  of  their  valuable  eliminative  properties,  and  the  acid  tartrate 
possesses  the  additional  advantage  of  acting  on  the  bowels  as  a 
hydragogue  saline  purgative. 

If  the  measures  already  mentioned,  in  conjunction  with  those 
about  to  be  described,  fail  to  afford  sufficient  relief  to  the  venous 
congestion  of  the  portal  and  systemic  circulations,  further  assist- 
ance must  be  rendered  to  the  heart  by  the  direct  removal  of  fluid 
from  the  oedematous  tissues,  and  by  drainage  of  ascitic  accumula- 
tion, or  pleural  effusion. 

These  operations  are  most  conveniently  and  safely  performed  by 
means  of  Southey's  tubes,  and  should  be  carried  out  with  the 
utmost  care  and  under  strict  antiseptic  precautions. 

The  relief  afforded  to  the  heart  by  the  removal  of  even  a  small 
quantity  of  fluid  in  any  of  these  situations  is  sometimes  remarkable, 
and  is  often  sufficient  to  turn  the  tide  of  events  in  the  direction  of 
recovery. 


DISEASES   OF   THE   MYOCARDIUM  287 

The  work  of  the  heart,  which  is  of  course  greatly  reduced  by 
complete  rest  in  bed,  may  be  still  further  Hghtened,  during  an 
emergency,  by  the  use  of  direct  arterial  dilators,  such  as  the  nitrites 
of  amyl  and  sodium,  nitro-glycerine,  erythrol  tetranitrate,  and  the 
spirits  of  nitrous  ether. 

Tlie  increase  in  tlie  contractile  power  of  the  heart. — Acute 
primary  dilatation,  or  urgent  failure  of  the  heart  from  any  cause, 
should  be  met  by  the  subcutaneous  injection  of  ether,  alcohol,  or 
strychnine,  which  is  the  most  rapid  and  potent  means  of  cardiac 
stimulation  that  we  possess. 

Less  serious  cases  may  be  treated  by  the  internal  administration 
of  half-drachm  doses  of  ether  and  sal  volatile,  in  combination  with 
four  or  five  minims  of  liquor  strychninse,  or  alcohol  may  be  given 
in  the  form  of  whisky  or  brandy. 

The  effect  of  these  remedies  can  be  supplemented  by  the  simul- 
taneous application  of  hot  turpentine  stupes  or  mustard  poultices  to 
the  praecordium,  or  of  ammonia  or  other  pungent  substance  to  the 
nose. 

Under  ordinary  circumstances,  however,  the  first  indication  in  the 
treatment  of  cardiac  failure  is  to  relieve  the  heart  of  work,  and  this 
must  be  done  in  the  manner  indicated  in  the  previous  section. 

The  systole  of  the  organ  can  then  be  strengthened  by  the  use  of 
cardiac  tonics,  which  may  when  necessary  be  prescribed,  at  first, 
with  stimulants  such  as  strychnine,  carbonate  of  ammonium,  or 
spirits  of  nitrous  ether. 

Later  they  may  be  advantageously  combined  with  iron,  arsenic, 
or  nux  vomica. 

The  most  important  of  the  cardiac  tonics  are  digitalis,  squill, 
senega,  strophanthus,  convallaria  majalis,  sparteine,  and  caffeine. 

Digitalis  is  the  most  powerful  as  well  as  the  most  generally  useful 
of  these  remedies,  and,  with  few  exceptions,  can  be  given  in  all 
forms  of  failure  of  compensation.  It  may  be  used  alone,  but  it  is 
often  more  efficacious  when  combined  with  squill  or  caffeine. 

It  is  worthy  of  notice  that  the  action  of  the  cardiac  tonics  is 
frequently  more  powerful  when  two  or  three  are  given  together  than 
when  the  same  drugs  are  prescribed  separately  and  successively. 

The  administration  of  digitalis  or  of  any  of  its  allies  should  always 
be  preceded  by  a  purge,  preferably  in  the  form  of  two  or  three  grains 
of  calomel  or  blue  pill,  with  half  a  drachm  or  more  of  compound 
jalap  powder. 

Next  to  digitalis  the  most  useful  cardiac  tonic  is  strophanthus. 
Given  alone,  or  in  combination  with  convallaria  majalis,  it  forms 
a  very  useful  substitute  for  digitalis  when  the  latter  drug  disagrees  or 
has  failed  to  do  good. 

The  use  of  squill  and  senega  as  cardiac  tonics  is  indicated  when 
an  expectorant  effect  is  also  desired,  in  which  case  either  or  both  of 
these  remedies  may  be  exhibited  in  combination  with  nux  vomica, 


288  DISEASES   OF   THE   HEART 

carbonate   of   ammonium,   and  other   cardiac   stimulants,   or   with 
other  expectorants. 

All  the  drugs  which  exert  a  tonic  influence  on  the  heart  act,  in 
addition,  on  the  kidneys  as  cardio-vascular  diuretics,  and  by  pro- 
moting a  free  flow  of  urine  they  assist  still  further  in  relieving 
venous  engorgement,  and  in  promoting  the  absorption  of  dropsical 
effusion. 

The  alleviation  of  pain  and  distress  and  the  promotion  of 
nutrition. — No  part  of  the  treatment  of  heart  failure  requires  more 
careful  consideration  than  the  use  of  sedatives,  and  there  are  no 
means  which  contribute  so  largely  to  the  comfort  and  well  being  of 
the  patient  as  the  skilful  and  proper  management  of  these  remedies. 
On  the  other  hand,  incalculable  harm  may  accrue  from  their  indis- 
criminate administration. 

Palpitation  and  prsecordial  pain  may  often  be  relieved  by  the 
local  application  of  hot  turpentine  stupes,  a  few  flying  blisters,  or 
a  belladonna  plaster.  The  internal  administration  of  belladonna, 
bromide  of  ammonium,  or  small  doses  of  opium  in  the  form  of 
Dover's  powder,  or  the  tincture,  may  be  used  for  the  same  purpose. 

Continuous  dyspnoea  or  orthopncea  is  sometimes  greatly  benefited 
by  the  subcutaneous  injection  of  a  small  dose  (gr.  -„-  to  i)  of  morphia. 
The  inhalation  of  oxygen  may  also  be  of  service  in  this  respect. 

Attacks  of  so-called  cardiac  asthma  may  be  treated  by  free  stimu- 
lation and  the  inhalation  of  nitrite  of  amyl.  In  severe  cases  relief 
can  be  obtained  by  the  subcutaneous  injection  of  morphia. 

Nitro-glycerine,  in  doses  of  one-hundredth  of  a  grain,  three  times 
a  day,  or  erythrol  tetranitrate,  in  half-grain  doses,  once  or  twice  a 
day,  may  be  given  in  the  interval  between  the  attacks. 

Insomnia  due  to  high  arterial  tension  is  relieved  by  the  adminis- 
tration of  one  or  two  grains  of  calomel  at  night.  In  some  instances 
sleep  cannot  be  obtained  except  in  the  semi-upright  position,  and 
when  this  is  the  case  much  can  be  done  to  make  the  patient  com- 
fortable by  the  use  of  a  suitable  bedchair,  or  other  means  of 
support. 

The  venous  engorgement  and  concurrent  catarrh  of  the  stomach 
and  intestines  greatly  interfere  with  the  processes  of  digestion  and 
assimilation,  consequently  the  feeding  of  the  patient  is  usually  a 
matter  of  considerable  difficult}'. 

Small  quantities  of  easily  digestible  food,  such  as  milk,  soup,  beef- 
tea  or  beef-jelly,  meat  extract  or  raw  meat  juice,  and  raw  eggs  beaten 
up  with  brandy,  may  be  given  every  three  or  four  hours  during  the 
day  and  night.  The  taste  of  raw  meat  juice,  which  is  a  particularly 
valuable  form  of  nourishment,  may  be  disguised  by  jam  or  gravy. 

There  is  no  objection  to  the  use  of  solid  food  provided  the 
patient  is  able  to  digest  it  without  discomfort. 

If   a  sufficient  quantity  of   nutriment  cannot  be  taken  by  the  - 
mouth,  the  amount  may  be  supplemented  by  rectal  alimentation. 


DISEASES    OF   THE    MYOCARDIUM         289 

For  this  purpose  two  ounces  of  fresh  or  peptonised  milk  should 
be  shaken  up  with  an  equal  quantity  of  beef-tea  and  a  raw  egg,  and 
the  mixture  is  then  slowly  and  gently  injected  into  the  bowel  once 
or  twice  a  day. 

Fluids  should  be  taken  sparingly,  more  especially  at  meals.  Thirst 
may  be  assuaged  by  sipping  toast-water,  or  the  preparation  known 
under  the  name  of  "imperial  drink,"  which  contains  the  acid  tartrate 
of  potassium  as  its  principal  ingredient. 

Alcohol  in  some  form  is  usually  required,  but  the  amount  must  be 
strictly  limited  by  the  requirements  of  each  individual  case.     It  is 
seldom  or  never  necessary  to  prescribe  more  than  ten  ounces  of/ 
brandy  or  whisky  in  the  twenty-four  hours. 


SECTION    II 
ACUTE   MYOCARDITIS 

iETIOLOGY 

Acute  inflammation  of  the  wall  of  the  heart  is  of  very  rare 
occurrence  as  a  primary  disorder,  and  when  apparently  observed 
as  such  its  mode  of  origin  is  usually  obscure,  though  chill  and  over- 
exertion have  in  some  instances  been  regarded,  with  doubtful 
accuracy,  as  the  exciting  causes. 

A  few  of  the  recorded  cases  have  followed  injury  to  the  chest 
wall  over  the  region  of  the  heart. 

With  these  exceptions,  acute  myocarditis  arises  in  the  course  of 
some  general  disorder,  such  as  acute  rheumatism,  and  is  then 
commonly,  though  not  always,  found  in  association  with  endocarditis 
or  pericarditis,  by  reason  of  the  direct  extension  of  the  inflammatory 
process  to  the  wall  of  the  heart,  or  as  part  of  a  general  "  carditis." 

It  sometimes  occurs  in  relation  with  other  acute  febrile  diseases, 
as,  for  instance,  diphtheria,  anthrax,  enteric  and  scarlet  fevers. 

A  large  proportion  of  the  cases  are  observed  in  connection  with 
pyaemia  due  to  acute  osteomyelitis,  and  other  suppurative  affections 
of  bones  and  joints,  puerperal  fever,  malignant  endocarditis,  and 
the  like. 

Pyemic  affections  of  the  cardiac  walls  are  most  commonly  found 
in  male  subjects  under  the  age  of  seventeen  years.  Thus  out  of 
fourteen  cases  collected  by  Sir  Richard  Quain,  twelve  occurred  in 
boys,  and  in  eleven  of  these  the  age  of  the  patient  did  not  exceed 
the  limit  just  mentioned. 

Myocardial  inflammation  is  occasionally  due  to  embolism  of  the 
branches  of  the  coronary  arteries,  and  in  very  rare  instances  it 
has  been  associated  with  malignant  disease  of  the  wall  of  tiie 
heart. 


290  DISEASES    OF   THE    HEART 


PATHOLOGICAL  ANATOMY 

Two  forms  of  acute  myocarditis  are  recognized,  according  as 
the  inflammatory  process  is  more  or  less  diffused  and  terminates 
in  fibrosis,  or  is  circumscribed  and  results  in  the  formation  of 
abscess. 

The  part  of  the  heart  involved,  in  either  event,  is  most  commonly 
the  wall  of  the  left  ventricle,  and  in  the  large  majority  of  cases 
inflammation  of  the  endocardium,  or  pericardium,  or  of  both  these 
membranes,  coexists  with  the  myocardial  lesion. 

In  the  diff"used  form  of  the  disease  the  affected  portion  of  the 
myocardium,  which,  at  first,  is  of  a  deep  red  or  purple  hue,  subse- 
quently becomes  reddish  grey  in  colour,  and  finally  presents  a  white, 
glistening,  tendon-like  appearance.  During  the  early  stages  of  the 
process  the  muscle  fibres  are  swollen  and  softer  than  normal. 

On  microscopical  examination  the  intermuscular  septa  are  seen 
to  be  infiltrated  with  leucocytes,  proliferated  connective  tissue  cells, 
and  sero-fibrinous  exudation.  The  blood  vessels  are  distended  and 
engorged  with  blood,  and  heemorrhages  are  not  infrequently  ob- 
served. The  muscle  cells  are  swollen  and  tend  to  split  up  trans- 
versely, while  the  normal  striation  of  the  fibres  is  indistinct  or 
altogether  lost  on  account  of  granular  and  fatty  degeneration  and 
nuclear  proliferation. 

The  subsequent  organization  of  the  inflammatory  products  leads 
to  further  compression  and  atrophy  of  the  muscle  fibres,  which 
become  wholly  or  partially  replaced  by  bands  or  patches  of  dense 
fibrous  tissue. 

In  rare  instances  the  muscular  tissue  has  been  found  either 
exclusively  or  predominantly  affected  by  inflammation,  and  to  this 
variety  of  the  disease  the  term  parenchymatous  myocarditis  has 
been  applied. 

Purulent  myocarditis  usually,  though  not  invariably,  arises  in 
connection  with  pyaemia,  and  appears  in  the  form  of  yellowish 
white  or  greyish  spots,  situated  immediately  beneath  the  endocar- 
dium, or  pericardium,  or  scattered  irregularly  throughout  the  wall 
of  the  heart. 

A  zone  of  hypersemia  surrounds  each  focus  of  inflammation, 
which  subsequently  develops  into  an  abscess  containing  pus  cells, 
granular  and  fatty  de'bris,  broken-down  muscular  tissue,  and  micro- 
organisms of  various  kinds. 

The  process  of  abscess  formation,  apart  from  pyaemia,  differs  in 
no  respect  from  that  already  described. 

General  suppuration  of  the  heart  is  of  very  rare  occurrence,  but 
it  is  not  uncommon  to  find  a  widespread  parenchymatous  degenera- 
tion of  the  muscular  substance  of  the  organ  in  association  with  the 
ordinary  form  of  the  disease. 


DISEASES    OF   THE    MYOCARDIUM  291 


PATHOLOGY 

The  results  of  acute  myocarditis  depend  on  the  nature,  intensity, 
and  extent  of  the  inflammatory  process. 

In  the  diffused  form  of  the  affection,  extensive  implication  of  the 
myocardial  substance  may  give  rise  to  acute  dilatation  of  the  heart, 
while  more  severe  and  limited  disease  may  be  followed  by  local 
bulging  of  the  wall  of  the  organ,  and  the  consequent  formation  of 
acute  cardiac  aneurism. 

Incompetence  of  the  auriculo-ventricular  valves  may  be  due  to 
inflammation  of  the  basal  muscular  ring  surrounding  these  orifices. 

Abscess  of  the  heart  may  burst  inwardly  into  the  ventricles  or 
auricles,  or  outwardly  into  the  pericardial  sac. 

In  the  first  event  the  contents  of  the  abscess  cavity  gain  access  to 
the  circulation,  and  may  be  the  source  of  general  pysemic  infection. 

Rupture  of  the  abscess  into  the  pericardial  sac  is  followed  by  acute 
suppurative  pericarditis. 

In  non-pysemic  cases  the  abscess  may  burst  both  in  an  inward 
and  outward  direction,  leading  to  rupture  of  the  heart  and  fatal 
haemorrhage  into  the  pericardial  cavity.  A  communication  between 
the  ventricles  or  auricles  may  be  established  by  the  rupture  of  an 
abscess  situated  in  the  interventricular  or  interauricular  septum. 


SYMPTOMS 

The  symptoms  of  acute  myocarditis  are  usually  more  or  less 
completely  masked  by  those  of  the  disease  with  which  the  myo- 
cardial lesion  is  associated.  Moreover,  when  symptoms  referable 
to  implication  of  the  muscular  substance  of  the  heart  are  observed, 
they  can  generally  be  more  easily  accounted  for  by  the  coexistence 
of  inflammation  of  the  pericardium  or  endocardium. 

In  well-marked,  uncomplicated  cases  the  patient  is  extremely 
restless,  and  complains  of  prsecordial  pain  and  uneasiness,  accom- 
panied by  dyspnoea,  palpitation,  and  irregular  tumultuous  action  of 
the  heart. 

There  is  usually  great  muscular  weakness  and  tremor.  The  ex- 
pression is  anxious,  the  face  and  lips  may  be  pale  or  cyanosed,  and 
the  extremities  are  frequently  cold  and  livid. 

Attacks  of  giddiness  or  faintness,  nausea,  vomiting  or  sweating, 
may  severally  or  collectively  arise  during  the  course  of  the  disease. 

The  fatal  termination  may  be  preceded  by  headache,  delirium, 
coma,  and  convulsions,  or  by  the  signs  and  symptoms  of  rapid 
failure  of  the  heart.  Sudden  death  is  sometimes  observed  as  the 
result  of  syncope  or  rupture  of  the  heart. 


292  DISEASES   OF   THE   HEART 


PHYSICAL  SIGNS 

The  physical  signs  of  acute  myocarditis  are  to  a  great  extent 
obscured  by  those  of  concurrent  inflammation  of  the  endocardium 
or  pericardium.  If,  however,  these  complications  can  be  excluded 
the  impulse  of  the  heart  is  found  to  be  feeble  and  diffused,  or 
altogether  impalpable.  The  area  of  cardiac  dulness  is  increased 
chiefly  in  the  lateral  direction.  The  sounds  of  the  heart  are  short 
and  weak,  and  the  first  sound  tends  to  become  gradually  fainter, 
so  that  finally  it  may  cease  to  be  audible.  Murmurs  may  be  heard 
in  different  situations,  but  they  present  no  special  features,  except 
in  cases  of  perforation  of  the  interventricular  septum,  when  a  bruit 
of  very  variable  character  is  suddenly  developed,  which  is  audible, 
as  a  rule,  over  the  greater  portion  of  the  pr^ecordial  area. 

The  pulse  is  rapid  and  irregular,  both  in  force  and  frequency, 
while  the  wave  is  small,  short,  and  badly  sustained. 


DIAGNOSIS 

The  existence  of  acute  myocarditis  is  usually  more  a  matter  of 
conjecture  than  of  actual  demonstration.  If,  as  is  rarely  possible, 
the  presence  of  both  endocarditis  and  pericarditis  can  be  ex- 
cluded, the  signs  and  symptoms  of  rapid  failure  of  the  heart, 
in  association  with  acute  rheumatism,  would  justify  a  diagnosis 
of  myocardial  inflammation.  Moreover,  when  endocarditis  or 
pericarditis  are  observed,  the  existence  of  myocarditis  may  be 
reasonably  suspected,  if  the  degree  of  cardiac  disturbance  is 
greater  than  can  be  fairly  accounted  for  by  the  inflammation  of 
the  endocardium  or  pericardium,  as  the  case  may  be. 

The  diagnosis  of  purulent  myocarditis  is  even  more  difficult  than 
that  of  the  simple  form  of  the  disease. 

The  sudden  appearance  of  a  murmur  indicative  of  rupture  of  the 
interventricular  septum,  followed  by  the  signs  and  symptoms  of 
general  pygemic  infection,  would  afford  strong  evidence  of  the 
existence  of  cardiac  abscess.  The  signs  of  valvular  rupture,  accom- 
panied by  a  similar  train  of  events,  would  not  have  the  same 
significance,  since  this  occurrence  may  likewise  be  due  to  malignant 
endocarditis. 

In  pysemic  cases  the  rapid  development  of  cardiac  failure,  with 
or  without  the  signs  of  acute  pericarditis,  might  lead  to  a  suspicion 
of  myocardial  inflammation. 

PROGNOSIS 

While  there  can  be  no  doubt  that  recovery  can  and  does  take 
place  after  slight  or  moderate  degrees  of  myocarditis,  it  is  equally 


DISEASES   OF  THE   MYOCARDIUM         293 

certain  that  the  diagnosis  of  the  lesion,  under  such  circumstances, 
is  seldom  or  never  made,  with  anything  like  precision,  during 
life. 

On  the  other  hand,  if  the  intensity  or  extent  of  the  myocardial 
inflammation  is  sufificient  to  give  rise  to  unmistakable  evidence  of 
its  existence,  the  outlook  is  most  unfavourable. 

In  cases  of  an  intermediate  character,  the  prognosis  rests  on  the 
degree  of  impairment  of  the  muscular  power  of  the  heart,  which 
must  be  gauged  by  a  careful  consideration  of  all  the  symptoms  and 
physical  signs  indicative  of  cardiac  insufficiency. 

Suppurative  myocarditis  is  almost  invariably  fatal  within  a  few 
days,  though  in  some  exceptional  instances  recovery  has  been 
accounted  for  by  the  inspissation  and  subsequent  calcification  of  the 
purulent  exudation. 

In  attem.pting  to  forecast  the  issue  of  acute  myocarditis,  the 
possibility  of  sudden  death  from  rupture  of  the  heart  must  be 
taken  into  account. 


TREATMENT 

The  treatment  of  acute  myocarditis  consists  mainly  in  the  removal 
of  the  cause ;  the  observance  of  complete  rest ;  the  alleviation  of 
cardiac  pain  and  excitement ;  and  the  maintenance  of  the  strength 
of  the  heart. 

The  use  of  salicylate  of  soda  in  the  treatment  of  acute  rheuma- 
tism, complicated  by  inflammation  of  the  myocardium,  requires  the 
utmost  caution,  on  account  of  the  depressing  influence  exerted  by 
this  drug  on  the  heart.  Salicin  is  less  objectionable,  but  both  these 
remedies  may  generally  be  replaced  with  advantage  by  quinine 
and  alkalies,  which  can  be  given  together  in  an  effervescing 
mixture. 

In  pysemic  cases  antiseptics  may  be  tried,  but  in  the  light  of 
recent  research  it  would  seem  preferable  to  employ  the  hypodermic 
injection  of  antistreptococcus  serum. 

Absolute  rest  in  bed  should  be  insisted  upon,  and  the  patient  must 
on  no  account  be  allowed  to  sit  up,  or  even  to  raise  himself.  Cardiac 
irritability  may  be  allayed  by  the  application  of  belladonna,  or  warm 
fomentations  to  the  praecordium,  and  the  internal  administration  of 
belladonna,  with  digitalis  or  strophanthus. 

Light  digestible  food  in  the  form  of  milk,  broth,  beef-tea,  or  beef- 
jelly,  raw  meat  juice,  etc.,  must  be  given  in  small  quantities  at 
frequent  intervals. 

Stimulants,  such  as  alcohol,  ether,  ammonia,  and  strychnine,  and 
cardiac  tonics  are  usually  imperatively  called  for,  but  their  use  must 
be  carefully  adjusted  to  the  requirements  of  the  heart,  since  over- 
stimulation of  the  organ  might  lead  to  rupture  of  the  softened 
walls. 


294  DISEASES   OF  THE    HEART 

SECTION    III 

DEGENERATIVE  DISEASES  OF  THE   MYOCARDIUM 

With  the  exception  of  parenchymatous,  fatty,  and  fibroid  affections, 
the  degenerative  diseases  of  the  muscular  walls  of  the  heart,  which 
comprise  changes  of  a  pigmentary,  amyloid,  hyaline,  and  calcareous 
nature,  possess  little  or  no  clinical  interest. 

The  precise  pathological  character  of  the  morbid  process  de- 
scribed here  as  parenchymatous  degeneration,  but  which  is  also 
known  under  the  names  of  granular  or  albuminous  degeneration, 
cloudy  swelling,  and  parenchymatous  or  infectious  myocarditis,  has 
not  yet  been  satisfactorily  determined.  By  some  it  is  regarded  as  a 
purely  degenerative  change,  a  view  shared  in  by  the  author  of  this 
work,  while  by  others  it  is  considered  to  be  of  an  inflammatory 
nature. 

The  mode  of  origin  of  the  condition  and  its  clinical  significance 
will  now  be  described  in  detail, 

PARENCHYMATOUS  DEGENERATION  OF  THE 

HEART 

AETIOLOGY 

This  form  of  degeneration  affects  chiefly  the  muscular  and  epi- 
thehal  tissues,  and  is  most  commonly  found  in  the  course  of  acute 
febrile  disorders,  such  as  enteric,  scarlet,  and  relapsing  fevers, 
diphtheria,  small-pox,  typhus,  erysipelas,  septicsemia,  and  pyaemia. 
It  also  occurs  in  connection  with  pneumonia,  acute  rheumatism, 
and  other  conditions  which  give  rise  to  long-continued  pyrexia. 

PATHOLOGICAL  ANATOMY 

The  heart  is  usually  more  or  less  dilated,  and  the  muscular  tissue 
of  the  organ,  which  is  diminished  in  consistence,  doughy  to  the 
touch,  and  more  friable  than  normal,  presents  on  section  a  pecuhar 
dull  greyish  yellow  tint.  The  endocardium  and  pericardium  may 
show  a  similar  change  of  colour. 

Under  the  microscope  the  normal  striation  of  the  affected  muscle 
fibres  is  seen  to  be  partially  or  wholly  obscured  by  a  finely  granular 
deposit,  which  is  irregularly  distributed  throughout  the  walls  of  the 
heart.  By  treatment  with  a  few  drops  of  glacial  acetic  acid,  or  a 
solution  of  potash,  the  granular  material  is  dissolved  and,  except 
that  they  remain  somewhat  swollen,  the  muscle  fibres  resume  an 
almost  natural  appearance. 

Nuclear  proliferation  of  the  muscle  cells  and  intermuscular  con- 
nective tissue  is  frequently  observed,  and  the  blood  vessels  in  the 
affected  areas  may  be  congested, 


DISEASES    OF   THE    MYOCARDIUM  295 

PATHOLOGY 

The  exact  mode  of  production  of  this  form  of  myocardial  de- 
generation is  still  a  matter  of  doubt.  It  has  been  attributed  to 
the  operation  of  the  pyrexia,  or  of  the  special  poison  associated 
with  the  different  ^etiological  conditions,  on  the  muscular  tissue  of 
the  heart.  It  has  also  been  regarded  as  a  post-mortem  change 
dependent  on  some  hitherto  unexplained  form  of  tissue  alteration 
during  life. 

In  whatever  manner  produced,  parenchymatous  degeneration  is 
frequently,  though  by  no  means  invariably,  the  immediate  precursor 
of  a  fatty  transformation  of  the  myocardium.  The  two  conditions 
may,  however,  be  easily  differentiated,  since  fatty  disease  is  unaffected 
by  the  reagents  mentioned  above,  whereas  it  is  easily  dissolved  by 
chloroform  and  ether,  which  exercise  no  visible  effect  on  parenchy- 
matous degeneration.  Moreover,  the  deposit  is  larger  and  more 
globular  in  the  event  of  fatty  change,  and  is  stained  black  by 
osmic  acid,  a  reaction  which  does  not  obtain  in  the  case  of  the 
parenchymatous  affection. 

Parenchymatous  degeneration  of  the  myocardium  seriously  weakens 
the  muscular  power  of  the  heart,  consequently  the  presence  of  the 
condition  is  a  factor  of  great  weight  in  the  prognosis  of  the  disease 
with  which  it  is  associated. 

SYMPTOMS  AND   PHYSICAL  SIGNS 

The  symptoms  of  parenchymatous  degeneration  of  the  muscular 
walls  of  the  heart,  though  seldom  well  defined,  are  those  of  cardiac 
insufficiency,  developing  during  the  course  of  one  of  the  acute 
specific  fevers.  They  are,  however,  of  little  or  no  use  in  the  diag- 
nosis of  the  lesion,  which  depends  mainly  on  the  evidence  afforded 
by  the  physical  signs.  A  careful  examination  of  the  heart  from  day 
to  day  in  the  course  of  an  acute  febrile  disorder,  such  as  enteric 
fever,  will  reveal  a  gradually  increasing  feebleness  of  the  cardiac 
impulse,  which  may  ultimately  be  altogether  imperceptible.  The 
first  sound  becomes  correspondingly  shorter  and  weaker,  and  may 
finally  disappear  or  be  replaced  by  a  soft  systolic  bruit. 

The  force  of  the  pulse  declines  with  the  increasing  enfeeblement 
of  the  muscular  power  of  the  heart,  and  in  advanced  degrees  of  the 
affection  the  beat  may  cease  to  be  palpable  at  the  wrist. 

DIAGNOSIS 

The  diagnosis  rests  on  the  occurrence  of  the  signs  just  described 
in  association  with  one  of  the  acute  specific  fevers  mentioned  under 
the  head  of  "Etiology." 

PROGNOSIS 

Parenchymatous  degeneration  of  the  cardiac  muscle  adds  greatly 
to  the  gravity  of  the  disease  of  which  it  is  a  complication.     The 


296  DISEASES   OF   THE    HEART 

degree  of  danger  corresponds  with  the  extent  and  rapidity  of  the 
enfeeblement  of  the  heart,  which  may  be  gauged  by  a  careful 
examination  of  the  condition  of  the  pulse,  cardiac  impulse,  and 
first  sound. 

TREATMENT 

The  occurrence  of  this  form  of  myocardial  degeneration  calls  for 
the  use  of  alcohohc  stimulants,  the  amount  of  which  must  be  regu- 
lated in  accordance  with  the  degree  of  cardiac  disability. 


SECTION    IV 

FATTY  DISEASE   OF   THE   HEART 

The  term  "fatty  disease  of  the  heart "  includes  two  distinct  patho- 
logical conditions,  which  are  distinguished  under  the  titles  of  "  fatty 
infiltration  "  and  "  fatty  degeneration  "  respectively.  The  mode  of 
origin  and  significance  of  the  two  affections  are  essentially  different, 
so  that  it  will  be  necessary  to  consider  them  separately. 

FATTY  INFILTRATION 

This  disease  is  characterised  by  an  increase  in  the  amount  of  sub- 
pericardial  fat,  which  oftentimes  penetrates  between  the  muscular 
fibres  of  the  heart. 

ETIOLOGY 

Fatty  infiltration  of  the  heart  is  most  commonly  observed  as  a 
local  manifestation  of  general  obesity,  but  it  is  occasionally  found 
in  connection  with  wasting  disorders,  such  as  malignant  and  tuber- 
culous affections. 

The  tendency  to  accumulate  fat  is  sometimes  hereditary,  though 
more  often  it  is  acquired  as  the  result  of  over-eating  and  over-drink- 
ing, in  association  with  an  insufficient  amount  of  exercise.  Fatty 
infiltration  of  the  heart  occurs  more  frequently  among  men  than 
women,  and  is  seldom  met  with  before  the  age  of  fifty. 

PATHOLOGICAL  ANATOMY 

In  well-marked  cases  the  heart  lies  embedded  in  a  covering  of 
fat,  which  extends  more  or  less  deeply  into  the  muscular  substance 
of  the  organ,  and  may  even  involve  the  columnae  carnese  and 
musculi  papillares.  The  overgrowth  of  fat  is  accompanied  by  a 
corresponding  amount  of  attenuation  of  the  myocardium,  so  that 
finally  the  wall  of  the  heart  may  appear  to  be  almost  wholly  con- 
verted into  adipose  tissue.     Under  the  microscope  the  pericardial 


DISEASES  OF  THE  MYOCARDIUM  297 

connective  tissue  is  seen  to  be  loaded  with  fat  cells,  which  invade 
the  myocardium  along  the  lines  of  the  intermuscular  septa.  The 
muscle  fibres,  more  especially  in  the  outer  portions  of  the  cardiac 
wall,  are  thinned  out  and  separated  by  wide  tracts  of  the  fatty  over- 
growth. The  course  of  the  fibres  may  be  variously  twisted,  but 
structurally  they  present,  as  a  rule,  a  perfectly  normal  appearance. 
In  very  advanced  cases,  however,  a  true  fatty  degeneration  of  the 
muscular  fibres  may  coexist  with  the  fatty  infiltration. 

PATHOLOGY 

The  relation  between  the  fatty  hyperplasia  and  the  atrophy  of 
the  muscle  fibres  is  still  uncertain,  though  there  appears  to  be  little 
doubt  that  it  is  not  one  of  cause  and  effect.  In  all  probability  the 
muscular  atrophy  is  the  primary  change,  and  is  followed  by  the 
fatty  overgrowth,  but  it  may  be  that  both  events  run  concurrently 
and  are  the  results  of  the  same  cause. 

The  accumulation  of  fat  on  the  surface  and  between  the  fibres 
of  the  heart  may  be  sufficient  to  seriously  hamper  the  movements 
of  the  organ,  but  the  chief  source  of  cardiac  weakness  arises,  no 
doubt,  from  the  atrophy  of  the  myocardium,  which  may  be  of  con- 
siderable extent. 

Great  thinning  of  the  muscular  parietes  may  be  followed  by 
rupture  of  the  heart. 

SYMPTOMS  AND  PHYSICAL  SIGNS 

Slight  degrees  of  fatty  infiltration  of  the  heart  give  rise  to  no 
symptoms  or  signs  by  which  the  disease  can  be  recognised,  with  any 
certainty,  during  life. 

The  condition  may,  however,  be  suspected  in  a  corpulent  in- 
dividual who  suffers  from  prsecordial  uneasiness  or  pain,  and  short- 
ness of  breath  on  slight  provocation,  with,  it  may  be,  paroxysms  of 
dyspnoea  or  attacks  of  faintness,  and  presents  in  addition  the  signs 
of  some  degree  of  cardiac  dilatation. 

The  symptoms  and  physical  signs  of  the  advanced  stages  of  the 
affection  resemble  those  of  fatty  degeneration  of  the  heart,  and  will 
be  described  under  that  heading. 

DIAGNOSIS 

The  diagnosis  of  fatty  infiltration  of  the  heart  rests  on  the  occur- 
rence of  the  symptoms  and  signs  of  cardiac  insufficiency  in  a  person 
of  corpulent  habit. 

PROGNOSIS 

In  attempting  to  forecast  tlie  issue  of  fatty  infiltration  of  the  heart 
it  is  necessary  to  take  into  consideration  the  amount  of  damage 
sustained  by  the  cardiac  muscle,  and  the  extent  to  which  repair 
is  likely,  as  well  as  the  effects  of  treatment  on  the  general  obesity. 
So  long  as  the  myocardium   is   sound,  and   provided   the   general 


298  DISEASES   OF   THE    HEART 

excess  of  fat  can  be  reduced  by  therapeutic  and  other  means,  the 
prognosis  will  be  favourable.  Extensive  atrophy  of  the  muscular 
parietes  of  the  heart  is  of  grave  import,  and  in  such  an  event  the 
possibility  of  sudden  death  from  syncope  or  rupture  of  the  thinned 
walls  must  not  be  lost  sight  of. 

TREATMENT 

The  objects  of  treatment  are  to  remove  or  reduce  the  general 
accumulation  of  fat,  to  sustain  the  strength  of  the  heart,  and  to 
improve  the  nutrition  of  the  cardiac  muscle. 

The  diet  must  be  carefully  regulated  with  the  view  of  restricting 
the  amount  of  starchy  and  fatty  foods,  and  of  maintaining  a  suitable 
proportion  of  proteids. 

Strict  moderation  should  be  observed  in  the  use  of  tobacco  and 
alcohol,  which,  in  the  form  of  spirits  and  malt  liquors,  must  be 
absolutely  prohibited. 

The  patient  should  be  encouraged  to  take  moderate  and  regular 
exercise  in  the  open  air,  and  the  action  of  the  skin  and  bowels  may 
be  assisted  by  diaphoretics  and  mild  saline  aperients. 

The  circulation  should  be  maintained  in  as  tranquil  a  condition  as 
possible,  and  all  sources  of  cardiac  strain  and  excitement  sedulously 
avoided. 

Graduated  muscular  exercise,  such  as  is  obtained  under  the  Schott 
and  CErtel  systems  of  treatment,  is  sometimes  of  very  great  service. 

The  action  of  alkalis,  and  of  the  salts  of  iron  and  iodine,  is  reputed 
to  be  of  service  in  the  treatment  of  general  obesity,  and  one  of  these 
remedies  may  be  employed  in  combination  with  some  general  tonic, 
such  as  arsenic,  strychnine,  or  quinine. 

Cardiac  tonics,  more  especially  digitalis,  must  be  given  with 
caution,  and  the  effects  should  be  carefully  noted. 

The  incidence  of  acute  intercurrent  disease  is  an  indication  for 
the  liberal  use  of  stimulants,  on  account  of  the  usual  inability  of  fat 
subjects  to  satisfactorily  withstand  shock  or  strain  of  any  kind. 

The  use  of  so-called  "  anti-fat "  remedies,  and  of  thyroid  extract 
in  the  treatment  of  obesity  is  not  unattended  by  danger. 

FATTY   DEGENERATION   OF  THE  HEART 

The  essential  feature  of  this  disease  is  a  fatty  transformation  of  the 
muscular  substance  of  the  heart. 

-ETIOLOGY 

Fatty  degeneration  ot  the  heart  is  due  to  interference  with  nutri- 
tion, more  particularly  with  the  process  of  oxidation,  which  may 
depend  either  on  an  impoverished  or  on  an  insufficient  supply  of 
blood  to  the  myocardium,  the  result  of  general  or  local  causes. 

Accordingly,  fatty  degeneration  of  the  heart  is  observed  in  con- 


DISEASES   OF  THE   MYOCARDIUM         299 

ditions  of  general  ansemia,  especially  pernicious  anaemia,  and  of 
poisoning  by  phosphorus,  and  it  may  be  by  arsenic,  antimony, 
mercury,  and  lead.  It  is  also  found  in  connection  with  long-con- 
tinued pyrexia,  and  the  puerperal  state,  and  occasionally  with 
chronic  cachectic  conditions  accompanying  prolonged  suppuration 
and  wasting  disorders. 

Interference  with  the  circulation  through  the  coronary  arteries 
constitutes  the  most  important  local  cause  of  fatty  degeneration 
of  the  heart.  This  may  be  due  to  atheromatous  disease  of  the 
coronary  arteries,  or  of  the  aorta  involving  the  orifices  of  these 
vessels,  or  it  may  depend  on  failure  of  the  left  ventricle  from 
any  cause. 

The  fatty  degeneration  of  the  cardiac  muscle  fibres  which  may  be 
observed  in  cases  of  enlargement  of  the  heart  is  occasioned  by  one 
or  other  of  these  conditions. 

Fatty  degeneration  of  the  heart  occurs  also  in  association  with 
acute  myocarditis,  and  more  especially  with  the  suppurative  variety 
of  this  affection.  a 

The  general  causes  of  fatty  degeneration  of  the  heart  are  usually 
operative  before  middle  life,  and  in  women  rather  than  in  men, 
while  fatty  degeneration  due  to  coronary  disease  is  rare  before  the 
age  of  sixty,  and  is  found  most  commonly  among  men. 

The  mode  of  origin  of  fatty  degeneration  of  the  heart  may  be 
contrasted  rather  than  compared  with  that  of  fatty  infiltration, 
since  the  one  is  the  result  of  under-nutrition,  the  other  of  over- 
nutrition. 

PATHOLOGICAL  ANATOMY 

The  morbid  appearances  vary  according  as  the  fatty  change  arises 
in  connection  with  general  causes,  and  is  widely  diffused  through 
the  wall  of  the  heart,  or  depends  on  local  conditions,  and  is  con- 
centrated at  one  or  more  spots. 

In  the  former  case  the  heart  is  usually  somewhat  enlarged,  more 
often  as  the  result  of  dilatation  than  of  hypertrophy,  but  it  may  not 
exceed  the  average  size,  and  is  sometimes  smaller  than  normal. 

The  muscular  substance  is  soft  and  friable,  and  of  a  light  brown 
colour,  interspersed  with  greyish  yellow  streaks  or  patches,  which 
correspond  with  the  sites  of  the  degenerative  changes.  The  parts 
most  affected  are  the  musculi  papillares  and  columns  carnese. 

In  typical  cases  these  structures  present  a  characteristic  transverse 
striation,  made  up  of  alternate  reddish  brown  and  pale  yellow 
markings,  an  appearance  that  has  been  likened  to  the  fur  of  a 
tabby  cat.  This  pecuhar  mottling  seen  through  the  endocardium 
is  not  observed  on  section  of  the  muscle,  the  cut  surface  of  which 
exhibits  a  uniform  yellowish  brown  or  buff  colour. 

On  microscopical  examination  the  irregular  distribution  of  the 
fatty  change  is  more  evident  than  it  is  to  the  naked  eye.  Fibres 
in  all  stages  of  degeneration  may  be  seen  running  side  by  side 


300  DISEASES   OF   THE   HEART 

with  others  that  are  perfectly  healthy.  The  morbid  change  appears 
at  first  in  the  form  of  minute  globules  of  fat,  collected  at  either  end 
of  the  nucleus,  or  scattered  in  clusters  throughout  the  substance  of 
the  muscle  cell. 

The  process  gradually  extends  until  finally  the  whole  structure 
of  the  fibre  is  completely  effaced  by  small  oil  globules,  which 
preserve  a  singular  uniformity  of  size  and  shape.  They  are  ulti- 
mately set  free  by  the  disintegration  of  the  affected  muscle  cells. 

In  the  local  form  of  the  disease  the  degenerative  changes  are 
confined  to  one  or  possibly  more  patches  of  variable  size,  situated 
usually  in  the  wall  of  the  left  ventricle.  The  affected  area  is  of 
a  yellowish  brown  colour,  breaks  down  easily  under  the  finger,  and 
may  exude  an  oily  fluid  on  pressure. 

The  microscopical  appearances  do  not  differ  from  those  already 
described,  except  that  relatively  a  larger  number  of  fibres  are 
affected  by  the  morbid  process. 

PATHOLOGY 

The  effects  of  fatty  degeneration  of  the  cardiac  muscle  are  to 
weaken  the  contractile  energy  of  the  heart,  and  to  diminish  either 
generally  or  locally  the  resisting  power  of  its  walls. 

The  result,  in  the  case  of  the  general  form  of  the  disease,  is 
the  production  of  a  variable  degree  of  dilatation  of  the  organ, 
which  may  be  attended  by  sudden  and  fatal  syncope.  This  event 
does,  however,  sometimes  happen  in  the  absence  of  any  enlargement 
of  the  heart. 

Local  weakness  of  the  cardiac  parietes  may  lead  to  aneurismal 
bulging,  or  to  rupture  of  the  wall  of  the  heart,  with  fatal  haemorrhage 
into  the  pericardial  sac. 

The  liability  to  sudden  death  from  one  of  the  causes  just 
mentioned  is  greater  in  this  form  of  heart  disease  than  in  any 
other. 

The  extent  to  which  repair  is  possible  in  cases  of  fatty  de- 
generation of  the  heart  is  not  known,  but  there  can  be  little  doubt 
that  shght  degrees  of  the  affection,  as,  for  instance,  those  due  to 
ansemia,  can  be  completely  recovered  from. 

SYMPTOMS 

The  symptoms  of  fatty  degeneration  of  the  heart,  more  especially 
of  the  early  stages  of  the  affection,  are  very  indefinite,  and  it  not 
infrequently  happens  that  the  disease  is  discovered  post-mortem 
without  any  evidence  of  its  existence  having  been  detected  during 
life.  In  such  cases  it  may  be  that  the  symptoms  due  to  impli- 
cation of  the  heart  are  merged  in  those  of  the  primary  disorder, 
and  thus  escape  observation,  or  that  the  organ,  though  crippled, 
is  still  equal  to  the  ordinary  requirements  of  the  circulation,  which, 


DISEASES    OF   THE    MYOCARDIUM         301 

under  the  circumstances,  are  usually  below  par.  In  the  latter 
event  a  comparatively  slight  cause,  such  as  moderate  exertion 
or  excitement,  may  be  sufficient  to  produce  arrest  of  the  heart's 
action  and  sudden  death. 

During  the  early  stages  of  the  disease  the  symptoms  are  for  the 
most  part  referable  to  cardiac  insufficiency,  and  do  not  differ  from 
those  of  commencing  dilatation  from  other  causes. 

Thus  the  patient  may  suffer  from  praecordial  pain,  palpitation, 
and  breathlessness  on  slight  exertion,  often  accompanied  by  a 
feeling  of  tightness  or  constriction  of  the  chest. 

Attacks  of  faintness  or  giddiness  are  sometimes  observed  to 
follow  even  a  moderate  amount  of  muscular  effort.  Want  of 
energy,  headache,  sleeplessness,  or  drowsiness  may  be  complained 
of,  and  are  indicative  of  disturbance  of  the  cerebral  circulation. 
As  the  disease  advances  the  symptoms  become  more  pronounced 
and  less  equivocal. 

The  shortness  of  breath  increases  and  tends  to  become  habitual, 
while  attacks  of  cardiac  asthma  and  angina  pectoris  may  occur 
from  time  to  time.  The  fatal  issue  may  be  preceded  by  the 
phenomenon  known  under  the  name  of  Cheyne-Stokes'  respira- 
tion. 

A  point  of  considerable  interest  and  significance  is  the  usual 
absence  of  well-marked  venous  congestion  or  serious  dropsy, 
though  it  cannot  be  said  that  this  peculiar  feature  of  the  disease 
has  been  satisfactorily  accounted  for. 

The  final  stages  of  fatty  degeneration  of  the  heart  are  character- 
ised in  some  instances  by  syncopal  attacks,  which  may  terminate 
fatally,  and  by  seizures  of  an  epileptic  and  apoplectic  nature.  In 
the  majority  of  cases  death  occurs  suddenly  from  syncope,  coma, 
or  rupture  of  the  heart. 

PHYSICAL  SIGNS 

Physiognomy. — A  white  satiny  or  greasy  condition  of  the  skin  has 
been  described  in  association  with  fatty  degeneration  of  the  heart, 
but  in  a  great  many  instances  the  patient  presents  a  fairly  healthy 
appearance,  even  up  to  the  time  of  death. 

The  presence  of  arcus  senilis  is  no  longer  considered  to  be  of 
importance  in  the  diagnosis  of  the  disease. 

Pulse. — The  pulse  is  usually  irregular  in  force  and  frequency,  and 
this  is  especially  noticeable  after  exertion.  The  radial  artery  is  of 
variable  size,  and  cannot,  as  a  rule,  be  felt  between  the  beats.  The 
wave  is  small,  sudden,  short,  and  badly  sustained.  The  pulse  rate 
may  occasionally  be  very  frequent  or  very  slow,  a  point  of  some 
diagnostic  value  in  either  event. 

Heart. — The  cardiac  impulse  is  feeble  and  diffused,  or  altogether 
impalpable.    The  area  of  percussion  dulness  may  be  increased,  chiefly 


302  DISEASES    OF   THE    HEART 

in  the  lateral  direction ;  on  the  other  hand,  it  is  often  of  normal 
extent. 

The  first  sound  at  the  apex  is  short  and  weak,  and  may  be  almost 
inaudible  in  advanced  stages  of  the  disease.  It  is  sometimes  accom- 
panied by  a  soft  systolic  murmur.  The  second  sound,  as  compared 
with  the  first,  is  often  clear  and  distinct. 

Disturbance  of  the  time  relations  between  the  sounds,  when 
observed,  is  always  in  the  direction  of  approximation. 

DIAGNOSIS 

There  are  no  symptoms  or  physical  signs  which  can  be  said  to  be 
characteristic  of  fatty  degeneration  of  the  heart.  Consequently  the 
diagnosis  of  the  condition  is  usually  a  matter  of  very  great  difficulty, 
and  is  seldom  made  with  much  certainty. 

The  occurrence  of  the  symptoms  and  signs  of  cardiac  insufficiency 
after  middle  age,  which  cannot  be  accounted  for  by  valvular  disease 
or  other  obvious  cause,  would  point  to  the  existence  of  myocardial 
degeneration.  This  indication  acquires  additional  significance  when 
associated  with  a  history  of  intemperance,  or  of  malnutrition  from 
other  causes,  and  with  the  presence  of  atheromatous  changes  in  the 
coats  of  the  accessible  arteries.  Under  circumstances  of  this  kind, 
the  appearance  of  symptoms  indicative  of  serious  cardiac  inadequacy, 
which  are  unaccompanied  by  the  signs  of  venous  congestion  and 
dropsy,  would  justify  a  diagnosis  of  fatty  degeneration  of  the  heart. 

PROGNOSIS 

The  prognosis  of  fatty  degeneration  of  the  heart  turns  for  the 
most  part  on  the  cause  and  extent  of  the  morbid  process.  If  the 
cause  can  be  discovered  and  is  removable,  as  may  happen  in  cases 
of  anaemia,  long-continued  pyrexia,  and  of  poisoning  by  various 
substances,  the  prospect  of  recovery  is  good. 

On  the  other  hand,  fatty  degeneration  of  the  heart  due  to 
obstruction  of  the  coronary  arteries  is  irremediable,  and  a  fatal 
termination  is  sooner  or  later  inevitable.  In  any  case,  the  attempt 
to  estimate  the  probable  duration  of  the  disease  must  be  qualified 
by  the  liability  to  sudden  death,  which  may  be  the  result  of  syncope 
or  rupture  of  the  heart. 

TREATMENT 

Treatment  must  be  directed  to  the  removal  of  the  cause  and  the 
improvement  of  the  general  health,  while  all  sources  of  cardiac 
strain  and  excitement  should  be  carefully  avoided. 

Malnutrition  of  the  heart,  due  to  anaemia  or  to  impoverishment 
of  the  blood  arising  in  other  ways,  calls  for  the  use  of  hsematinics 
and  general  tonics,  the  action  of  which  may  be  supplemented  by 
suitable  hygienic  and  dietetic  means. 


DISEASES    OF   THE    MYOCARDIUM         303 

The  treatment  of  the  myocardial  changes  associated  with  febrile 
conditions  will  be  found  under  the  head  of  parenchymatous  de- 
generation of  the  heart. 

In  the  local  form  of  the  disease,  which  is  due  to  obstruction  in 
the  coronary  circulation,  little  or  nothing  can  be  effected  in  the  way 
of  the  removal  of  the  cause,  but  much  may  be  done  to  promote  the 
comfort  of  the  patient,  and  to  prolong  life. 

It  is  of  the  first  importance  that  all  sources  of  cardiac  strain,  such 
as  bodily  or  mental  effort,  excitement,  anxiety,  and  especially  sudden 
exertion,  should,  so  far  as  practicable,  be  avoided. 

Exercise  on  the  level  ground  may  be  permitted,  and  will  be 
beneficial,  provided  it  does  not  give  rise  to  pain  or  shortness  of 
breath. 

The  patient  must  be  warmly  clad,  and  he  should  take  care  not  to 
expose  himself  to  cold. 

Dietetic  treatment  consists  in  the  use  of  light  nutritious  food, 
which  should  be  taken  in  moderate  quantities,  and  at  regular 
intervals.  Alcohol,  tea,  and  coffee  may  be  taken  sparingly,  while 
tobacco  should  be  altogether  prohibited. 

A  daily  evacuation  of  the  bowels  is  desirable,  and  should  be 
effected  by  mild  aperients.  The  use  of  strong  purgatives  for  this 
purpose  is  not  unattended  by  danger. 

Treatment  by  drugs  is  seldom  of  much  service,  though  the 
administration  of  general  tonics,  such  as  iron,  arsenic,  and  strych- 
nine, appears  to  do  good  in  some  cases.  Benefit  is  occasionally 
derived  also  from  the  use  of  digitalis,  but  this  drug  and  its  allies 
must  be  employed  with  caution,  on  account  of  the  increased  strain 
which  their  action  may  impose  on  the  weakened  cardiac  walls. 

Dyspepsia  and  flatulence  may  be  a  source  of  discomfort  and 
danger,  and  their  occurrence,  in  spite  of  a  careful  regulation  of  the 
diet,  must  be  met  by  prompt  and  vigorous  treatment  in  the  shape  of 
stomachic  carminatives  and  antiseptics  in  combination  with  nux 
vomica  and  general  stimulants. 

Failure  of  the  heart  is  an  indication  for  the  liberal  administration 
of  alcohol,  in  the  form  of  whisky  or  brandy,  with,  if  necessary, 
ether,  ammonia,  and  strychnine. 

In  other  respects  treatment  may  be  conducted  on  the  lines  laid 
down  under  the  head  of  cardiac  dilatation. 


SECTION  V 

FIBROID   DISEASE   OF   THE   HEART 

.ETIOLOGY 

Fibroid  disease  of  the  heart  may  depend  on  a  diffused  or  circum- 
scribed hyperplasia   of  the  intermuscular   fibrous    tissue,   or   on  a 


304  DISEASES    OF    THE    HEART 

localized  necrosis  of  the  cardiac  wall  (myomalacia  cordis)  with 
subsequent  regeneration  and  fibrosis. 

A  variety  of  the  general  form  of  the  disease,  described  by  Sir 
Richard  Quain  under  the  title  of  "  connective  tissue  hypertrophy 
of  the  heart,"  has  been  attributed  to  over-feeding.  With  this  excep- 
tion, a  diffuse  intermuscular  fibrosis  of  the  myocardium  is  found  in 
association  with  long-continued  venous  congestion  of  the  heart,  or 
with  disease  of  the  kidneys. 

A  circumscribed  fibroid  change  is  sometimes  the  sequel  of  an 
acute  interstitial  myocarditis,  or  it  may  be  due  to  the  extension 
along  the  intermuscular  septa  of  a  chronic  indurative  process,  that 
has  originated  in  inflammation  of  the  endocardium  or  pericardium. 

In  the  majority  of  cases,  however,  circumscribed  fibroid  disease 
of  the  heart  arises  in  connection  with  myomalacia  cordis,  which  is 
the  result  of  an  ansemic  necrosis,  or,  in  other  words,  of  infarction 
of  the  cardiac  wall,  consequent  on  obstruction  of  the  coronary 
circulation. 

This  condition  may  depend  on  atheroma,  endarteritis  obliterans, 
or  embolism  of  the  coronary  arteries  and  their  branches,  and  is 
therefore  most  commonly  observed  among  males  in  relation  with 
old  age,  gout,  alcoholism,  chronic  Bright's  disease,  syphilis,  and 
prolonged  muscular  exertion. 

Syphilitic  disease  of  the  wall  of  the  heart  occurs  also  in  the  form 
of  a  patchy  interstitial  fibrosis,  which  may  be  the  result  of  a  simple 
inflammatory  induration  of  the  myocardium,  or  of  gummatous 
changes. 

PATHOLOGICAL    ANATOMY 

A  diffuse  interstitial  fibrosis  of  the  myocardium  is  usually  found 
in  association  with  great  enlargement  of  the  heart,  wherein  hyper- 
trophy and  dilatation  are  variously  combined.  The  walls  of  the 
organ,  which  may  be  thickened  or  thinned,  are  of  a  peculiar  tough 
leathery  consistence,  and  do  not  collapse  on  section.  Under  the 
microscope  the  intermuscular  fibrous  overgrowth  may  be  observed 
in  all  stages  of  development,  from  small  round  and  spindle  cells 
to  wavy  bands  of  fibrillse.  The  muscular  tissue  may  present  a 
perfectly  normal  appearance,  or  may  be  in  some  stage  of  granular  or 
fatty  degeneration. 

The  circumscribed  form  of  the  disease  appears  in  the  shape  of 
streaks,  bands,  or  patches  of  yellowish  or  greyish  white  fibrous 
tissue,  situated  in  the  substance  of  the  myocardium,  most  commonly 
near  the  apex,  or  in  some  other  portion  of  the  wall  of  the  left 
ventricle.  Implication  of  the  right  ventricle  is  usually  due  to  the 
extension  of  the  morbid  process  from  the  left  side  of  the  heart. 

The  amount  of  fibrous  material  and  its  mode  of  distribution 
are  subject  to  considerable  variation.  Thus  it  may  lie  deeply 
embedded  in  the  muscular  tissue  of  the  heart,  so  that  it  is  seen 
only  on  section  of  the  organ,  or  it  may  replace  more  or  less  com- 


DISEASES   OF   THE    MYOCARDIUM         305 

pletely  the  entire  thickness  of  the  cardiac  wall  over  a  considerable 
area.  In  other  instances  it  appears  as  a  local  opaque  thickening 
immediately  below  the  endocardium  or  pericardium,  whence  it 
radiates,  in  the  form  of  streaks  or  bands,  between  the  adjacent 
muscle  fibres.  At  the  same  time,  the  endocardium  or  pericardium, 
or  both  these  membranes,  are  commonly  the  seat  of  the  chronic 
inflammatory  changes.  Adhesion  between  the  two  layers  of  the 
pericardium,  whether  general  or  partial,  is  always  most  dense  and 
firm  at  the  spot  where  the  fibroid  material  reaches  the  outer  surface 
of  the  heart,  and  is  not  infrequently  limited  to  this  situation. 

Thrombosis  may  occur  over  the  corresponding  site  on  the  endo- 
cardial surface. 

A  localized  fibrosis  of  the  papillary  muscles  is  not  uncommon, 
while  in  rare  instances  the  entire  column  may  undergo  a  fibroid 
transformation.  This  change  has  no  relation  with  the  fibrous 
thickening  that  is  observed  at  the  apices  of  these  structures,  in 
common  with  the  valves  and  chordae  tendines,  in  cases  of  long- 
continued  high  intra-cardiac  tension. 

The  wall  of  the  heart  over  a  fibroid  patch  is  usually  more  or  less 
thinned,  but,  on  the  other  hand,  an  increase  in  thickness  is  some- 
times found. 

Under  the  microscope  the  normal  structure  of  the  myocardium, 
in  the  affected  area,  is  seen  to  be  largely  replaced  by  dense  fibrous 
tissue,  containing  few  cellular  elements.  In  the  central  portions 
of  the  diseased  patch  all  trace  of  muscular  substance  may  have 
disappeared,  while,  at  the  margins,  the  bundles  of  muscle  fibres  are 
separated  by  wide  tracts  of  the  fibroid  growth.  The  atrophy  of 
the  muscle  cells  is  not  accompanied  by  any  well-marked  structural 
alteration,  though  granular  and  fatty  changes  are  occasionally 
observed. 

PATHOLOGY 

The  effects  of  fibroid  disease  of  the  heart  vary  with  the  extent 
and  site  of  the  morbid  process.  A  general  interstitial  fibrosis  of 
the  myocardium  must  interfere  more  or  less  with  the  functional 
activity  of  the  heart,  and  consequently  is  accompanied  by  hyper- 
trophy and  dilatation  of  the  organ,  though,  for  obvious  reasons,  the 
latter  condition  usually  preponderates. 

A  like  result  may  follow  the  circumscribed  form  of  the  disease, 
more  especially  if  it  is  of  considerable  extent.  On  the  other  hand, 
a  localized  fibrosis  of  the  myocardium,  if  small  in  amount,  may 
exist  without  giving  rise  to  any  alteration  in  the  size  of  the  heart  or 
even  to  any  appreciable  functional  disturbance.  Implication  of  the 
papillary  muscles  may  be  a  cause  of  valvular  incompetence. 

An  important  effect  of  circumscribed  fibroid  disease  is  the  local 
weakening  of  the  cardiac  parietes,  which  most  commonly  affects 
some  portion  of  the  wall  of  the  left  ventricle.  The  diseased  area 
may  give  way  before  the  intra-ventricular  pressure,  so  that  a  local 

X 


3o6  DISEASES    OF  THE    HEART 

bulging  or  aneurism  of  the  wall  is  produced,  which  may  mechanically 
interfere  with  the  movements  of  the  heart,  or  may  lead  to  sudden 
death  by  the  bursting  of  the  sac.  A  communication  between  the 
two  ventricles  is  sometimes  due  to  the  rupture  of  an  aneurism  of 
the  interventricular  septum. 

Cardiac  aneurism  is  of  exceedingly  rare  occurrence,  except  as  the 
result  of  fibroid  disease  of  the  heart.  In  some  instances  the  fibroid 
material  undergoes  contraction,  instead  of  expansion,  with  the  pro- 
duction of  a  puckered  cicatrix  of  the  cardiac  wall,  or  of  narrowing 
of  one  or  other  of  the  orifices  of  the  heart. 

Annular  contraction  of  the  conus  arteriosus,  arising  in  this  way, 
is  known  under  the  name  of  "stenosis  of  the  heart." 

SYMPTOMS 

The  symptoms  of  fibroid  disease  of  the  heart  are  very  indefinite. 
In  some  instances  the  affection  is  unaccompanied  by  any  appreciable 
functional  disturbance  of  the  organ,  while  in  others  the  first  and 
only  indication  of  the  existence  of  the  lesion  is  sudden  death. 

The  abrupt  cessation  of  the  heart's  action  under  such  circum- 
stances has  not  yet  been  satisfactorily  explained. 

In  the  majority  of  cases,  however,  the  symptoms  of  the  disease 
are  practically  identical  with  those  of  cardiac  dilatation  and  in- 
sufficiency due  to  other  causes,  and  comprise  dyspnoea  on  exertion, 
palpitation,  and  prsecordial  pain  or  distress,  followed  sooner  or 
later  by  cough,  haemoptysis,  and  the  signs  of  pulmonary  congestion, 
general  venous  engorgement  and  dropsy. 

Attacks  of  syncope,  cardiac  asthma,  and  angina  pectoris  are  some- 
times prominent  features  of  the  affection. 

Fibroid  disease  of  the  heart  generally  runs  a  chronic  course,  and 
terminates  with  the  usual  signs  and  symptoms  of  cardiac  failure. 
Sudden  death  is  sometimes  observed  as  the  result  of  rupture  of  an 
aneurism  of  the  heart,  or  of  embolism  of  one  of  the  coronary 
arteries. 

PHYSICAL  SIGNS 

Physiognomy. — There  is  nothing  characteristic  about  the  appear- 
ance of  patients  suffering  from  fibroid  disease  of  the  heart,  though  a 
variable  degree  of  cyanosis  may  be  developed  with  the  occurrence 
of  failure  of  the  organ. 

Pulse. — The  pulse  is  usually  irregular,  both  in  force  and  frequency, 
a  feature  that  has  been  held  to  be  of  some  diagnostic  value.  A 
very  slow  pulse  rate,  not  exceeding  thirty  beats  to  the  minute,  is 
occasionally  observed.  In  other  respects  the  characters  of  the  pulse 
do  not  differ  from  those  associated  with  cardiac  failure  from  other 
causes. 

Heart. — Physical  examination  generally  reveals  the  existence  of 
enlargement  of  the  heart,  which  as  a  rule  is  mainly  due  to  dilatation. 


DISEASES    OF   THE    MYOCARDIUM  307 

Careful  percussion  might  in  some  instances  map  out  an  area  of 
dulness  suggestive  of  cardiac  aneurism.  The  first  sound  at  the  apex 
may  be  accompanied  by  a  systolic  murmur  due  to  mitral  in- 
competence, which  may  depend  on  dilatation  of  the  left  ventricle 
or  on  fibrosis  of  the  papillary  muscles. 

DIAGNOSIS 

The  diagnosis  of  fibroid  disease  is  at  all  times  a  matter  of  very 
great  difficulty,  and  in  the  present  state  of  our  knowledge  impossible 
in  the  majority  of  cases. 

When  it  is  possible  to  exclude  other  sources  of  heart  weakness, 
such  as  valvular  lesions  and  the  extra-cardiac  causes,  the  occurrence 
of  enlargement  and  insufficiency  of  the  organ  in  association  with 
general  arterial  disease  would  point  to  the  probable  existence  of 
fibroid  degeneration  of  the  myocardium.  This  indication  would  be 
supported  by  evidence  of  pericardial  adhesion,  or  of  syphilis. 

PROGNOSIS  . 

When  the  diagnosis  of  fibroid  disease  of  the  heart  can  be  made, 
the  prognosis  is  most  unfavourable. 

TREATMENT  -v'V^^ 

Treatment  can  be  palliative  only,  and  should  be  conducted  on 
.the  general  principles  described  under  dilatation  of  the  heart. 

All  sources  of  cardiac  strain  and  excitement  should  be  sedulously 
avoided,  and  tranquillity  of  the  circulation  promoted  by  rest  and 
other  appropriate  hygienic  and  dietetic  means. 

Digestive  derangements  should  be  promptly  rectified,  and  the 
bowels  carefully  regulated. 

Little  benefit  is  derived  from  the  use  of  drugs,  though  arsenic  and 
iodide  of  potassium  seem  occasionally  to  be  of  service. 

Digitalis  must  be  prescribed  cautiously,  in  view  of  the  harmful 
effects  that  sometimes  have  been  observed  to  follow  the  adminis- 
tration of  the  drug  in  cases  of  this  kind. 

In  the  treatment  of  heart  failure,  reliance  should  preferably  be 
placed  on  cardiac  stimulants,  such  as  ether,  alcohol,  ammonia,  and 
strychnine,  which  must  be  given  in  quantities  suitable  to  the  require-  ^^ 
ments  of  the  occasion. 


SECTION  VI 

GROWTHS   IN   THE   HEART 

Among   the   morbid   growths  which   may   attack  the  heart   are 
carcinoma,    sarcoma,    tubercle,    syphilis,    lymphadenoma,    myoma, 


3o8  DISEASES    OF   THE    HEART 

fibroma,  lipoma,  hydatid  cyst,  and  cysticercus.  All  these  conditions 
are  rare,  some  exceedingly  so,  and  are  interesting  from  a  patho- 
logical rather  than  from  a  clinical  point  of  view.  The  more  common 
and  important  growths  only  will  be  briefly  considered. 


MALIGNANT   DISEASE 

Both  carcinoma  and  sarcoma  are  almost  invariably  secondary  to 
similar  lesions  in  other  parts  of  the  body,  though  a  few  instances 
of  primary  implication  of  the  heart  are  on  record.  In  some  cases 
the  organ  is  invaded  by  the  direct  extension  of  the  growth  from 
a  primary  focus  in  the  mediastinum,  lungs,  or  stomach. 

Carcinoma  occurs  in  the  encephaloid,  scirrhous,  or  epithelio- 
matous  form,  while  sarcoma  may  be  of  the  lympho-sarcomatous 
or  melanotic  variety. 

The  morbid  growth,  in  either  case,  is  usually  multiple,  and 
appears  most  commonly  immediately  beneath  the  endocardium 
or  pericardium,  though  the  substance  of  the  myocardium  is  some- 
times involved. 

Implication  of  the  endocardium  or  pericardium  may  be  associated 
with  inflammation  of  these  structures. 

The  right  side  of  the  heart  is  said  to  be  more  commonly  the 
seat  of  malignant  disease  than  the  left. 


TUBERCLE 

Tubercular  disease  of  the  myocardium  apart  from  a  similar 
affection  of  the  pericardium  is  exceedingly  rare.  Miliary  tubercles 
have  been  observed  in  the  intermuscular  connective  tissue  in  cases 
of  acute  general  tuberculosis.  In  other  instances  the  disease  has 
appeared  in  the  form  of  sub-pericardial  caseous  nodules. 


HYDATID   CYST 

The  heart  is  sometimes  the  seat  of  hydatid  cysts,  which  may 
be  single  or  multiple,  and  are  situated  in  the  substance  of  the 
myocardium  on  either  side  of  the  organ.  The  tumour  may  project 
either  inwards  or  outwards,  and  may  rupture  in  either  or  both 
of  these  directions.  In  other  cases  the  sac  may  lead  to  obstruction 
of  one  or  other  of  the  cardiac  orifices,  or  to  incompetence  of  the 
valvular  structures. 

SYPHILIS 

The  manifestations  of  this  disease  with  respect  to  the  heart 
have  already  been  referred  to  under  fibroid  degeneration  of  the 
myocardium. 


DISEASES    OF   THE    MYOCARDIUM  309 


LYMPHADENOMA 

The  heart  is  sometimes  involved,  in  common  with  the  other 
organs  of  the  body,  in  cases  of  general  lymphadenoma. 

Non-malignant  tumours  of  the  heart  are  exceedingly  rare,  and 
possess  no  clinical  interest. 

SYMPTOMS 

In  a  large  number  of  the  cases  of  cardiac  neoplasmata  no 
symptoms  have  been  present.  Malignant  disease  of  the  heart  has 
occasionally  been  associated  with  severe  prtecordial  pain.  When 
the  lungs  are  affected  by  the  morbid  growth  as  well  as  the  heart, 
cough,  haemoptysis,  and  dyspnoea  are  prominent  symptoms. 

PHYSICAL  SIGNS 

Evidence  of  pericarditis  is  sometimes  obtained  in  cases  of 
malignant  and  tubercular  disease  of  the  heart.  In  other  instances 
the  tumour  gives  rise  to  obstruction  of  an  orifice  or  to  incom- 
petence of  a  valve,  and  in  this  way  may  be  accompanied  by  the 
signs  and  symptoms  of  valvular  disease. 

DIAGNOSIS 

The  diagnosis,  which  is  hardly  ever  made,  rests  on  the  occurrence 
of  the  signs  and  symptoms  of  cardiac  insufficiency  in  connection 
with  the  presence  of  a  new  growth  in  some  other  portion  of  the 
body. 

PROGNOSIS 

If  it  were  possible  to  make  a  diagnosis  of  a  new  growth  in  the 
heart,  a  fatal  prognosis  only  could  be  given. 

TREATMENT 

Treatment  consists  in  the  relief  of  pain  and  distress,  which  may 
be  effected  by  the  measures  indicated  in  previous  sections  of  this 
work. 


CHAPTER   XXIII 
ANGINA   PECTORIS 

Etiology — Kinds  of  Angina — Morbid  Anatomy — Pathogenesis — Symptoms— ^ 
Physical  Signs — Diagnosis — Prognosis — Treatment, 

"Anguish  of  the  heart"  is,  perhaps,  the  best  paraphrase  of  this 
term. 

i^TIOLOGY 

In  the  present  state  of  our  knowledge  of  angina  pectoris  it  is 
difficult  to  give  a  systematic  account  of  the  aetiology,  morbid 
anatomy,  and  pathology  of  this  condition,  but  an  attempt,  which 
must  be  regarded  as  tentative,  will  be  made  to  consider  the  disease 
under  these  heads. 

Angina  pectoris  in  the  form  originally  portrayed  by  Heberden  is 
a  rare  disorder.  It  occurs,  in  the  large  majority  of  cases  among 
men,  between  the  ages  of  forty  and  sixty-five.  Statistics  show  that 
the  proportion  of  men  to  women  attacked  by  the  disease  is  about  as 
ten  to  one. 

The  incidence  of  angina  pectoris  exhibits  a  marked  hereditary 
tendency. 

Physical  and  mental  strain,  gout,  rheumatism,  syphiHs,  and 
plumbism  are  ^etiological  factors  in  so  far  as  they  are  concerned 
in  the  production  of  cardio-vascular  disease. 

Any  of  the  conditions  (see  p.  79)  which  raise  arterial  tone,  and 
thereby  increase  arterio-capillary  resistance,  also  act  as  contributory 
causes  of  angina  pectoris. 

The  abuse  of  alcohol  and  tobacco  exerts  a  causal  influence  in 
that  the  action  of  these  drugs  in  excess  gives  rise  not  only  to  nervous 
disturbance  of  the  heart  and  vaso-motor  mechanism,  but  also  to 
organic  disease  of  the  cardio-vascular  system. 

A  certain  number  of  cases  of  angina  pectoris  have  been  observed 
to  follow  influenza. 

The  chief  exciting  cause  of  the  attack  is  physical  exertion.  A 
comparatively  small  muscular  effort,  more  especially  when  made 
suddenly,  is  oftentimes  sufficient  to  bring  on  a  paroxysm.  Emotional 
disturbance,  particularly  in  the  form  of  anger  or  nervous  shock,  is 

310 


ANGINA   PECTORIS  311 

also  a  potent  means  of  exciting  an  attack.  Among  other  important 
proximate  causes  of  the  disease  are  indigestion  with  flatulent  disten- 
sion of  the  stomach,  constipation,  and  cold  applied  to  the  surface  of 
the  body,  i.e.  by  cold  winds,  or  by  bathing. 

Two  forms  of  angina  pectoris  are  recognised,  viz. : — 

1.  True  angina  pectoris 

2.  False  angina  pectoris 

So  far  the  aetiology  of  true  angina  pectoris  only  has  been  con- 
sidered. 

False  angina  pectoris,  or  pseudo-angina  pectoris,  or  angina  pec- 
toris vasomotoria,  as  it  is  now  commonly  designated,  is  subdivided 
into  two  groups,  the  neurotic  and  the  toxic. 

The  neurotic  variety  occurs  at  any  age,  but  is  most  prevalent 
between  puberty  and  middle  life.  Women  are  rather  more  com- 
monly affected  than  men.     An  hereditary  tendency  is  well  marked. 

Occupations  involving  nervous  strain  predispose  to  the  occurrence 
of  this  form  of  angina  through  the  vaso-motor  disturbance  to  which 
they  so  frequently  give  rise. 

Any  of  the  conditions  which  lead  to  increased  arterio-capillary 
resistance  may  be  connected  with  the  causation  of  angina  pectoris 
vasomotoria. 

Influenza  has  appeared  to  exert  a  causal  influence  in  some  cases. 

The  toxic  form  of  pseudo-angina  is  ascribable  to  the  abuse  of  tea, 
cofifee,  tobacco,  etc. 

Huchard  distinguishes  three  forms  of  tobacco  angina,  viz. : — 

1.  A  form  due  to  functional  spasm  of  the  coronary  arteries,  pro- 

duced by  the  direct  action  of  the  drug  on  the  vaso-motor 
mechanism  of  the  heart. 

2.  A  form  due  to  arterial  spasm  consequent  on  the  dyspepsia 

produced  by  tobacco. 

3.  A  form   due   to   arterio-sclerosis   with   narrowing   of  vessels, 

produced  by  chronic  tobacco  poisoning. 

One  of  the  most  important  exciting  causes  of  an  attack  of  pseudo- 
angina,  in  all  its  forms,  is  chilHng  of  the  surface  of  the  body,  which 
may  be  brought  about  by  exposure  to  cold  winds,  by  immersion  in 
cold  water,  by  insufficient  covering  during  sleep,  etc.  Mental 
emotion,  physical  exertion,  dyspepsia  with  flatulence  and  constipa- 
tion, are  also  frequent  exciting  causes  of  pseudo-angina. 


312  DISEASES   OF   THE   HEART 


MORBID  ANATOMY 

True  angina  pectoris  is  associated  with  a  great  many  different 
morbid  conditions  of  the  heart  and  vessels,  which  may  be  briefly 
classified  as  follows  : — 

1.  Disease  of  the  endocardium. — Aortic  incompetence  is  the 
valvular  affection  most  commonly  found.  Aortic  stenosis  is,  how- 
ever, not  infrequently  observed,  and  in  very  rare  instances  mitral 
stenosis  has  been  noted. 

2.  Disease  of  the  pericardium. — Adherent  pericardium  is  occa- 
sionally present,  but  always  in  association  with  aortic  valvular 
disease. 

3.  Disease  of  the  myocardium. — Fatty  infiltration  of  the  cardiac 
wall  is  sometimes  found  independent  of  disease  of  the  coronary 
vessels. 

In  the  great  majority  of  cases,  however,  lesions  of  the  cardiac 
wall  depend  on  arterio-sclerosis  (atheroma)  of  the  coronary  arteries 
and  their  branches,  or  on  aortic  disease  involving  the  orifices  of  one 
or  both  of  these  vessels. 

The  coronary  arteries  and  their  branches  become  partially  or 
wholly  occluded,  or  converted  into  rigid  and  thickened  calcareous 
tubes,  with  a  corresponding  degree  of  interference  with  the  blood 
supply  to  the  wall  of  the  heart. 

The  more  important  morbid  changes  which  are  produced  by 
interference  with  the  coronary  circulation  are  fatty  infiltration  and 
fatty  degeneration  of  the  cardiac  wall,  fibroid  or  fatty  fibroid  disease 
of  the  heart,  and  hsemorrhagic  infarction  or  softening  of  the  cardiac 
muscle. 

The  heart  is  usually  enlarged,  and  its  walls  soft  and  flaccid. 

4.  Disease  of  the  aorta  and  systemic  arteries. — The  aorta  is 
commonly  the  seat  of  atheromatous  disease,  which  may  involve  the 
orifices  of  the  coronary  arteries. 

Aortitis  usually  gives  rise  to  angina.  Dilatation  of  the  ascending 
portion  of  the  aorta  is  frequently  found,  and  in  some  instances 
there  is  an  aneurism  of  the  vessel.  The  systemic  arteries  com- 
monly show  arterio-sclerotic  (atheromatous)  changes. 

5.  Disease  of  the  cardiac  plexuses  and  ganglia. — In  a  few 
instances  pigmentary,  granular,  and  other  degenerative  changes 
have  been  found  in  the  vagi,  cardiac  plexuses,  and  cardiac  ganglia. 

It  is  stated  that  in  some  fatal  cases  of  angina  pectoris  a  careful 
examination  of  the  heart  and  vessels  has  failed  to  reveal  any  sign  of 
disease. 

Pseudo-angina  pectoris  has  no  morbid  anatomy. 


ANGINA   PECTORIS  313 


PATHOLOGY 

Since  the  morbid  conditions  of  the  heart  and  systemic  arteries 
enumerated  above  are  found  much  more  commonly  without  than 
with  the  symptoms  of  angina  pectoris,  it  is  clear  that  they  operate  as 
contributory  causes  only  of  the  attack. 

The  central,  indeed  the  essential,  feature  of  angina  pectoris  is  the 
inability  of  the  heart  for  the  time  being  to  adequately  perform  its 
work,  and  it  is  from  this  standpoint  that  the  pathology  of  the  two 
varieties  of  the  disease  can  be  profitably  compared  and  harmonized. 

In  angina  pectoris,  of  whatever  variety,  the  inability  of  the  heart 
to  cope  with  its  work  may  depend  on — 

1.  Mural  weakness  (absolute  or  relative). 

2.  Increased  peripheric  resistance. 

3.  A  combination  of  mural  weakness  and  increased  peripheric 

resistance. 

Now,  the  morbid  changes  found  in  the  cardiac  wall  in  connection 
with  angina  pectoris  are  not  evenly  distributed  throughout  the  heart. 
In  other  words,  the  areas  of  disease  and  the  lesions  of  the  coronary 
vessels,  or  their  branches,  are  scattered  irregularly  throughout  the 
wall  of  the  ventricles,  auricles,  and  aorta. 

It  may  be  pointed  out  also,  that  the  nervous  tissue  {i.e.  ganglia 
and  nerve  fibres)  distributed  over  the  wall  of  the  heart  probably 
suffers  in  common  with  the  muscular  substance  of  the  organ. 

If,  now,  stress  be  thrown  on  the  heart,  the  areas  of  diseased  wall 
are  unable  to  take  their  share  in  resisting  the  increased  intra-cardiac 
pressure,  and  consequently  become  unduly  stretched  and  distended. 

Again,  a  coronary  artery,  or  one  or  more  of  its  branches,  is  the 
seat  of  atheromatous  disease,  whereby  the  vessel  or  vessels  become 
thickened  and  rigid,  or  partially  occluded. 

The  areas  of  distribution  of  the  affected  vessels  may  be  sufficiently 
supplied  with  blood  so  long  as  the  heart  is  acting  quietly.  So  soon, 
however,  as  stress  is  imposed  on  the  organ  the  diseased  vessels  are 
unable  to  satisfy  the  additional  demand  for  blood,  and  the  muscle 
fibres  in  the  areas  supplied  are  thus  temporarily  thrown  out  of  action, 
and  in  consequence  become  unduly  stretched  and  distended  by  the 
increased  intra-cardiac  pressure. 

The  pain  felt  under  these  circumstances  is  accounted  for  by  the 
stretching  and  tension  of  the  nerve  elements  in  the  areas  involved, 
and  it  has  already  been  pointed  out  that  these  structures  are,  in 
all  probability,  unusually  impressionable  and  irritable. 

The  distribution  of  the  pain  is  explained  by  the  connection  of  the 
sensory  nerves  of  the  heart  and  aorta  with  the  spinal  cord  from  the 
third  cervical  to  the  eighth  dorsal  roots.  The  overflow  of  sensory 
nerve  stimuli  from  the  heart  appears  to  travel  chiefly  along  the 


314  DISEASES   OF   THE   HEART 

second  dorsal  roots,  which  are  in  connection  with  the  left  ventricle, 
where  presumably  the  pain  most  commonly  originates. 

The  sense  of  impending  death  which  is  a  characteristic  feature  of  a 
fully  developed  attack  of  angina  pectoris  is  readily  explained  by  the 
hypothesis  under  consideration.  It  is  obvious  that  if  distension  and 
stretching  of  localized  areas  of  the  cardiac  wall  take  place  during 
systole  the  ventricular  parietes  are  simultaneously  undergoing  con- 
traction and  expansion.  The  effect  of  this  dynamical  perversion  of 
the  cardiac  movements  on  the  impressions  transmitted  to  the  cardiac 
centre  during  the  ventricular  contraction  must  be  contradictory  and 
antagonistic.  The  cardiac  centre  must  under  these  circumstances 
be  thrown  into  a  turmoil,  and  herein  lies  the  explanation  of  the  sense 
of  impending  death.  The  disturbance  of  the  cardiac  centre  spreads  to 
adjacent  centres  whereby  it  becomes  possible  to  explain  the  nausea, 
flatulence,  hiccough,  etc.,  that  are  so  commonly  associated  with  the 
anginal  paroxysm. 

The  occurrence  of  sudden  death  is  explicable  on  the  assumption 
that  the  arrival  at  the  cardiac  centre  of  equally  balanced  antagonistic 
impulses  inhibits  the  action  of  the  centre. 

The  view  advanced  here  will  explain  the  occurrence  of  the  so- 
called  angina  pectoris  sine  dolore  (Gairdner)  as  an  occasional  mode 
of  termination  of  true  angina  pectoris.  The  absence  of  pain  in  these 
cases  is  due  to  the  fact  that  the  whole  ventricular  wall  becomes 
in  course  of  time  more  or  less  evenly  affected  by  disease,  so  that 
no  particular  area  or  areas  are  unduly  stretched  during  a  rise  of 
intra-cardiac  pressure.  The  patient  dies  from  syncope  or  from  rapid 
dilatation  and  failure  of  the  heart. 

In  pseudo-angina  the  cause  of  the  attack  lies  in  the  increased 
peripheric  resistance,  and  the  rise  of  intra-cardiac  pressure  produced 
thereby  is  evenly  distributed  over  the  inner  surface  of  the  left 
ventricle,  so  that  the  symptoms  are  those  of  acute  distension  of 
the  heart. 

If,  now,  a  portion  of  the  cardiac  muscle  be  insufficiently  supplied 
with  blood  as  a  consequence  of  spasm  of  one  of  the  coronary 
arteries  or  its  branches,  the  conditions  for  the  production  of  some 
degree  of  anginal  pain  are  in  all  probability  present,  for  the  reasons 
already  given. 

It  is  possible,  indeed  most  probable,  that  spasm  of  the  coronary 
arteries  (which  are  affected  in  common  with  the  rest  of  the' arterial 
system)  plays  the  same  role  in  the  production  of  the  phenomena 
of  pseudo-angina  that  organic  disease  of  these  vessels  does  in  the 
causation  of  an  attack  of  true  angina  pectoris. 

On  these  lines,  therefore,  the  two  forms  of  angina  pectoris  merge 
imperceptibly  into  one  another. 

A  brief  account  of  the  various  other  theories  which  have  been  ad- 
vanced to  explain  the  phenomena  of  angina  pectoris  must  now  be 
given. 


ANGINA   PECTORIS  315 

1.  Heberden  ascribed  the  disease  to  spasm  of  the  heart. 

In  view  of  the  morbid  changes  found  in  the  cardiac  walls  after 
death,  such  a  condition  of  affairs  must  be  a  physical  impossibility. 

2.  The  disorder  has  been  attributed  to  acute  distension  of  the 

heart  consequent  on  the  strain  to  which  the  organ  is  exposed 
in    its    endeavour    to   cope   with   the    increased    peripheral 
resistance. 
This  view  has  been  fortified  by  taking  into  account  concomitant 

spasm  of  the  coronary  arteries,  which,  by  temporarily  restricting  the 

blood  supply  to  the  cardiac  muscle,  adds  to  the  embarrassment  of 

the  heart. 

There  is  little  doubt  'that  this  explanation  holds  good  so  far  as 

the    phenomena   of  angina    pectoris  vasomotoria  (Nothnagel)   are 

concerned. 

3.  Angina  pectoris  has  been  regarded  as  a  neuralgia,  or  even 

neuritis  of  the  cardiac  nerves,  by  many  eminent  authorities. 
A  modification  of  this  view  suggests  that  the  disease  is  a  neuralgia 
superimposed  on  an  organic  basis,  or  that  it  is  a  cardiac  neuralgia 
or  neurosis  in  connection  with  disturbed  innervation  of  the  vaso- 
motor mechanism. 

4.  An  old  theory  revived  (first  promulgated,  according  to  Osier, 

by  Allan  Burns  in  1809)  attributes  the  phenomena  of  the 

attack    to    cramp    of    the    cardiac    muscle    consequent    on 

restricted   arterial   blood   supply.     The   diminution    of   the 

blood    supply,    which    is    felt    during    increased    functional 

activity  only,  depends  on  the  narrowing   of   the   coronary 

arteries  produced  by  arterio-sclerosis  (atheroma). 

The  parallel  of  this  condition  in  the  case  of  the  skeletal  muscles, 

is  described  by  Bouley  under  the  title  of  "  intermittent  claudication," 

and  is  characterized  by  loss  of  power  and  painful  cramp-like  seizures 

in  the  muscles  of  the  limbs  and  other  parts.     Here,  owing  to  the 

partial  or  complete  occlusion  of  the  nutrient  vessels  by  disease, 

the  blood  supply  to   the   affected  muscles  is   inadequate   for   the 

«  display  of  even  a  moderate  degree  of  functional  activity,  though 

|(  it  may  be  sufficient  during  rest  or  slight  exertion. 

The  loss  of  power  and  pain  experienced  both  in  the  case  of  the 
.     heartland  skeletal  muscles  is  attributable  to  the  same  cause,  viz. 
an  iiBufiicient  supply  of  arterial  blood  and  the  consequent  accumu- 
lation of  waste  products  in  the  muscular  tissue. 

Under  physiological  conditions,  the  functional  activity  of  muscular 
tissue  is  attended  by  dilatation  of  its  blood  vessels,  which  not  only 
admits  an  increased  supply  of  oxygen,  but  also  hastens  the  removal 
of  waste  products.  It  is  this  process  which  is  at  fault  under  the 
circulatory  conditions  which  obtain  in  angina  pectoris,  for  obviously 
the  thickened  and  rigid  coronary  vessels  are  unable  to  respond  by 
changes  in  calibre  to  the  requirements  of  the  cardiac  muscle. 


3i6  DISEASES  OF  THE  HEART 


SYMPTOMS 

Although  the  symptoms  of  the  two  forms  of  angina  pectoris  are 
in  all  probability  similar  in  pathogenesis,  it  mil  be  convenient,  for 
purposes  of  description  and  of  differential  diagnosis,  to  consider 
them  separately. 

The  symptoms  which  characterize  an  attack  of  true  angina  pectoris 
are  as  follow  : — 

The  patient,  usually  while  engaged  in  some  trivial  exertion,  or 
during  emotional  excitement— less  commonly  after  exposure  to  cold 
or  after  a  full  meal,  but  occasionally  during  perfect  rest — is  suddenly 
seized  with  severe  pain  in  the  region  of  the  heart.  The  pain,  which 
varies  in  intensity  in  different  cases,  is  always  agonizing,  and  is 
described  by  the  patient  as  tearing,  rending,  crushing,  or  stabbing 
in  character.  In  other  instances  the  sensation  is  as  if  the  chest 
were  gripped  in  a  vice,  or  as  if  the  sternum  were  being  forced  back 
on  the  spine.  The  pain  usually  commences  in  the  prjecordial 
region,  and  radiates  backwards  to  the  spine,  and  upwards  to  the 
left  side  of  the  neck  and  left  shoulder ;  thence  down  the  inner  side 
of  the  left  arm  as  far  as  the  elbow,  but  rarely  beyond  this  joint. 
Less  commonly  the  pain  extends  over  both  sides  of  the  chest  and 
neck  and  down  both  arms,  and  in  cases  of  exceptional  severity  it 
travels  downwards  over  the  abdomen  to  the  testes  and  lower 
extremities. 

The  aspect  of  the  patient  is  expressive  of  intense  suffering  and 
mental  distress,  and  reflects  the  sense  of  impending  death,  which 
is  the  dread  accompaniment  of  the  pain.  A  pallid  grey  hue  spreads 
over  the  face,  the  lips  become  livid  in  colour,  and  a  cold,  clammy 
sweat  breaks  out  on  the  forehead. 

With  the  onset  of  the  paroxysm  the  sufferer  generally  remains 
rooted  to  the  spot,  not  daring  to  move  or  even  take  a  deep  breath.  ^ 
In  other  instances  he  assumes  some  posture,  such  as  leaning  over  a 
the  back  of  a  chair,  kneeling,  lying  down,  etc.,  which  instinct  or 
experience  suggests  will  bring  relief. 

The  breathing  is  hurried  and  shallow,  and  each  short  inspffation 
appears  to  bring  little  or  no  relief  to  the  distressing  sense  of  air 
hunger  which  is  experienced.  The  patient  may  feel  faint  and  giddy 
during  the  attack,  but  with  very  few  exceptions  consciousness  is 
retained.  Flatulence,  vomiting,  dysphagia,  loss  of  voice,  and  an 
overpowering  desire  to  make  water  occasionally  form  part  of  the 
paroxysm. 


Angina  pectoris  31; 


PHYSICAL  SIGNS 

The  action  of  the  heart  is  usually  slightly  increased  in  frequency, 
and  it  may  be  irregular.  In  some  cases  the  action  of  the  heart  has 
been  said  to  be  undisturbed.  The  cardiac  impulse  is  feeble,  while 
the  sounds  of  the  heart  are,  as  a  rule,  short,  sharp,  and  weak. 
Adventitious  sounds  in  the  form  of  murmurs  may  or  may  not  be 
observed. 

The  pulse  is  most  commonly  increased  in  frequency,  irregular, 
small  in  volume  and  force,  and  ill-sustained,  reflecting  thus  the  weak 
condition  of  the  left  ventricular  impulse. 

In  some  instances  arterial  tone  is  Increased,  and  the  pulse  gives 
evidence  of  heightened  tension  ;  that  is,  the  vessel  is  full  between 
the  beats  and  not  easily  compressible. 

In  other  cases  the  pulse  shows  the  condition  described  by 
Sir  William  Broadbent  as  "virtual  tension,"  that  is,  a  condition 
which  would  be  high  tension  if  only  the  heart  were  strong  enough 
to  cope  with  the  increased  peripheral  resistance. 

Cutaneous  hypersesthesia,  in  the  shape  of  tenderness,  can  be 
elicited  in  the  praecordial,  postcordial,  and  supra-orbital  regions 
in  cases  of  angina  pectoris. 


COURSE  AND  TERMINATIONS 

The  duration  of  the  attack  varies  considerably.  It  may  last  for 
a  few  seconds,  or  it  may  continue  for  five,  ten,  or  fifteen  minutes, 
and  in  very  rare  instances  it  may  extend  over  hours.  As  a  rule, 
the  duration  of  the  paroxysm  is  measured  by  seconds  or  a  few 
minutes  only. 

The  attack  usually  ceases  as  abruptly  as  it  begins.  The  termina- 
tion is  frequently  signalized  by  the  eructation  of  gas  from  the 
stomach,  accompanied,  it  may  be,  by  an  urgent  desire  to  micturate. 
it  will  be  noticed  that  distension  of  the  stomach  by  gas  is  an  effect 
ktp  well  as  a  cause  of  angina  pectoris.  The  patient  is  usually  more 
or  less  exhausted  after  a  paroxysm. 

The  first  attack  sometimes  ends  fatally,  but  more  commonly  it 
terminates  in  recovery,  in  which  case  the  patient  may  remain  free 
from  the  disease  for  many  years,  or  possibly  for  the  rest  of  his  life. 
The  seizures  tend,  however,  to  increase  in  frequency  and  severity, 
as  well  as  to  be  more  easily  excited. 

It  sometimes  happens  that  the  patient  is  able  to  ward  off  or  cut 
short  a  paroxysm,  by  immediately  discontinuing  movement,  or  by 
taking  drugs  the  moment  the  premonitory  symptoms  of  the  attack 
are  experienced. 

Angina  pectoris  usually  terminates  sooner  or  later  in  sudden 
death  during  a  paroxysm.     A  certain  number  of  the  cases  develop 


3i8  DISEASES  OF  THE  HEART 

syncopal  attacks  without  pain  (angina  pectoris  sine  dolore),  in  one  of 
which  they  die.  In  some  instances  gradual  failure  of  the  circula- 
tion is  the  cause  of  death,  and  according  to  Balfour  this  is  the 
usual  mode  of  termination  of  angina  pectoris. 

In  pseudo-angina,  or  angina  pectoris  vasomotoria,  the  attack,  which 
is  commonly  excited  by  cold  or  emotion,  begins  quite  suddenly 
with  pain  and  oppression  in  the  region  of  the  heart,  and  coldness 
or  numbness  of  the  extremities.  The  pain  may  radiate  over  the 
chest  and  upper  extremities,  but  is  not  so  severe  as  in  true  angina, 
and  though  it  may  be  accompanied  by  a  feeling  of  anxiety  and 
mental  distress,  the  apprehension  of  immediate  death  is  not  ex- 
perienced. The  sense  of  air-hunger  is  a  marked  feature  of  the 
attack,  and  there  is  frequently  a  good  deal  of  restlessness  and 
struggling  for  breath.  The  face  is  pale  and  the  expression  anxious, 
and  the  extremities  are  commonly  cold  and  livid. 

The  action  of  the  heart  is  excited,  and  there  is  usually  accentua- 
tion of  the  aortic  second  sound. 

The  pulse  is  frequently  irregular  in  force  and  frequency,  the 
artery  is  small  and  can  usually  be  felt  between  the  beats ;  the  pulse 
wave,  though  small,  is  not  easily  obliterated  by  pressure  with  the 
fingers. 

The  attacks  are  of  short  duration,  seldom  lasting  longer  than  a 
few  seconds  or  a  few  minutes  at  the  most.  The  subsidence  of  the 
paroxysm  is  usually  marked  by  the  discharge  of  a  large  quantity 
of  urine. 

The  attacks  tend  to  occur  in  groups,  with  long  periods  of  com- 
plete immunity  between  them. 


DIAGNOSIS 

The  diagnosis  of  angina  pectoris  seldom  presents  much  difficulty 
provided  the  characteristic  features  of  the  attack  are  developed. 
The  peculiar  nature  of  the  pain,  its  sudden  onset  and  abrupt 
cessation,  its  remarkable  distribution,  together  with  the  terrible 
sense  of  impending  death,  form  a  group  of  symptoms  that  are 
quite  distinctive. 

In  cases  of  doubt  the  various  extra-cardiac  conditions,  which, 
by  giving  rise  to  paroxysmal  attacks  of  pain,  may  simulate  the 
agony  of  angina  pectoris,  have  to  be  excluded. 

A  careful  consideration  of  the  symptoms  and  signs  would  suffice 
to  distinguish  the  pain  associated  with  hepatic,  renal,  or  intestinal 
colic  from  the  pain  excited  by  the  cardiac  lesion. 

The  chief  difficulty  is  connected  with  the  differentiation  between 
the  organic  and  functional  forms  of  angina  pectoris.  The  main 
points  in  the  differential  diagnosis  are  as  follow  : — 

True  angina  is  rare  before  forty-five  years  of  age,  apart  from 


ANGINA  PECTORIS  319 

aortic  regurgitation,   aortitis,   and  aneurysm.     On  the  other  hand, 
pseudo-angina  may  occur  at  any  age. 

True  angina  rarely  affects  women  at  any  period  of  Hfe.  The 
exciting  cause  of  the  attack  has  considerable  diagnostic  significance. 
True  angina  is  most  commonly  brought  about  in  the  first  instance 
by  exertion,  whereas  pseudo-angina  comes  on  spontaneously  during 
rest,  or  occurs  after  food,  or  exposure  to  cold. 

The  phenomena  of  the  attack  with  respect  to  the  severity  of  the 
symptoms,  as  shown  by  the  appearance  and  behaviour  of  the  patient, 
are  of  importance,  in  that  the  absence  of  the  facial  expression  of 
pain  and  alarm  would  be  evidence  in  favour  of  the  incidence  of  the 
functional  form  of  the  disease. 

Moreover,  pseudo-angina  is  commonly  associated  with  other 
symptoms  of  nervous  disturbance,  whereas  this  is  not  usually  the 
case  with  respect  to  true  angina.  Evidence  of  vaso-motor  disturb- 
ance is  more  commonly  obtained  in  relation  with  pseudo-angina,  but 
its  presence  does  not  exclude  true  angina. 

It  must  be  borne  in  mind  that,  even  after  the  most  exhaustive 
analysis  of  the  symptoms  and  signs,  the  diagnosis  sometimes  re- 
mains in  doubt. 


PROGNOSIS 

The  attempt  to  forecast  the  course  and  duration  of  angina  pectoris 
is  fraught  with  many  difficulties.  Speaking  generally,  the  outlook 
is  favourable  in  proportion  to  the  extent  to  which  the  cause  of  the 
paroxysms  can  be  mitigated  or  removed. 

If  the  attack  depends  on  disease  of  the  cardiac  wall  alone,  the 
prognosis  is  bad.  On  the  other  hand,  if  the  exciting  cause  can  be 
shown  to  be  exertion,  indigestion,  etc.,  it  is  possible  by  the  careful 
avoidance  of  these  conditions  to  put  off  the  attacks  indefinitely. 
Again,  habitually  high  arterial  tone  can  be  lessened  by  suitable 
treatment,  and  in  this  way  the  work  of  the  heart  can  be  reduced. 

The  more  easily  the  attacks  are  excited  the  greater  the  danger. 

The  prognosis  of  pseudo-angina  is  favourable  as  regards  the 
danger  to  life,  but  in  view  of  the  occasional  difficulty  of  differenti- 
ating between  the  two  forms  of  angina,  it  is  well  to  give  a  guarded 
prognosis  in  these  cases. 


TREATMENT 

The  objects  of  treatment  in  angina  pectoris  are  (i)  the  relief  of 
the  paroxysms,  and  (2)  the  removal  or  mitigation  of  the  conditions 
upon  which  the  paroxysms  depend. 

In  the  treatment  of  the  attacks  it  is  important  to  discover,   if 


320  DISEASES    OF   THE    HEART 

possible,  whether  the  inability  of  the  heart  to  perform  its  work 
is  due  to  {a)  increased  peripheric  resistance,  {b)  weakness  of  the 
cardiac  walls,  (c)  a  combination  of  the  two  conditions  just  men- 
tioned, or  {d)  interference  with  the  action  of  the  heart  by  a  distended 
stomach,  etc.,  in  conjunction  with  increased  peripheric  resistance  or 
cardiac  weakness. 

If  the  pulse  tension  be  high  during  the  paroxysm,  three  or  four 
minims  of  a  one  per  cent,  solution  of  nitro-glycerine  by  the  mouth, 
or  five  to  ten  minims  of  amyl  nitrite  by  inhalation,  will  relax  the 
peripheral  vessels,  and  will  thus  bring  immediate  relief  to  the  heart 
by  reducing  the  stress  in  front.  This  plan  of  treatment  is  often 
brilliantly  successful  in  bringing  the  paroxysm  to  an  end. 

When  there  is  no  evidence  of  increased  arterial  tone  and  the 
symptoms  point  to  cardiac  weakness  only,  the  best  remedy  is  the 
subcutaneous  injection  of  three  or  four  minims  of  liq.  strychninae. 
Ether,  ammonia,  or  brandy  may  also  be  used  to  stimulate  the  heart 
under  these  circumstances. 

A  combination  of  any  of  these  remedies,  with  a  few  minims  of 
a  one  per  cent,  solution  of  nitro-glycerine,  will  meet  the  requirements 
of  a  weak  heart  acting  against  increased  peripheric  resistance. 

Distention  of  the  stomach  can  be  removed  by  the  administration 
of  carminatives,  such  as  peppermint  or  oil  of  cloves,  or  by  a  draught 
of  the  compound  spirits  of  ether,  or  the  aromatic  spirits  of  ammonia. 
In  extreme  cases  the  condition  can  be  relieved  by  the  use  of  the 
oesophageal  tube. 

If  these  methods  of  treatment  fail  to  do  good,  opium,  given 
preferably  in  combination  with  atropine,  either  by  the  mouth  or 
by  subcutaneous  injection,  relieves  the  pain  and  gives  the  heart 
time  to  recuperate  by  rest- 

The  inhalation  of  oxygen  is  sometimes  of  very  great  service  in 
relieving  the  sense  of  air-hunger  which  is  frequently  a  prominent 
feature  of  the  paroxysm. 

An  attack  of  angina  pectoris  vasomotoria,  when  due  to  cold,  can 
be  relieved  by  the  application  of  warmth  to  the  extremities  in 
conjunction  with  vigorous  friction  of  the  limbs. 

The  treatment  of  pseudo-anginal  attacks  should  be  conducted  on 
the  lines  already  indicated  in  the  case  of  true  angina 

After  the  subsidence  of  the  paroxysm  the  whole  case  must  be 
thoroughly  investigated  with  the  object  of  elucidating  the  cause 
of  the  disease. 

Errors  of  diet  must  of  course  be  corrected,  and  indigestion  treated 
by  appropriate  remedies.  The  food,  which  should  contain  a  fair 
proportion  of  nitrogenous  principles,  must  be  light  and  easily 
digestible.  The  quantity  of  food  taken  at  one  meal  should  be 
moderately  restricted,  and  a  period  of  rest  after  eating  must  be 
insisted  upon. 

The  use  of  alcohol,  tea,  tobacco,  etc.,  must  be  carefully  regulated, 
and  in  some  instances  entirely  prohibited. 


ANGINA  PECTORIS  321 

Exercise  in  the  open  air  is  of  the  utmost  importance,  but  care 
must  be  observed  that  the  amount  of  exertion  undertaken  is  well 
within  the  limits  of  the  cardiac  powers.  Under  no  circumstances 
should  exercise  be  carried  to  the  point  of  fatigue. 

Mental  strain  and  excitement  is  likewise  prejudicial,  and  the 
patient  should  also  be  warned  against  exposure  to  cold  and  wet. 
The  bowels  should  be  carefully  regulated,  since  constipation  is 
sometimes  an  exciting  cause  of  the  attack. 

The  chief  indication,  so  far  as  the  therapeutic  treatment  of 
angina  pectoris  is  concerned,  is  the  control  and  reduction  of  arterial 
tone. 

The  methods  by  which  undue  resistance  in  the  arterio-capillary 
circulation  can  be  reduced  and  kept  under  control  are  already 
familiar  to  the  reader. 

Provided  the  heart  exhibits  even  a  moderate  degree  of  vigour, 
a  mild  mercurial  laxative  taken  once  or  twice  a  week  is  of  the 
utmost  service  in  reducing  arterial  blood  pressure.  The  iodide  and 
bicarbonate  or  citrate  of  potassium  can  also  be  used  for  the  same 
purpose,  and  in  combination  with  nux  vomica  or  arsenic  are  the 
most  useful  drugs  for  continuous  administration. 

Among  the  direct  vaso-dilators  the  most  suitable  drug  for  pro- 
longed use  is  erythrol  tetranitrate,  given  in  half  to  one  grain  doses 
twice  daily. 

A  course  of  phosphorus  is  sometimes  of  great  service  in  the 
treatment  of  angina  pectoris. 

The  treatment  of  aortic  disease,  when  complicated  by  angina 
pectoris,  should  be  conducted  on  general  principles. 

The  medicinal  treatment  of  pseudo-angina  consists  in  the  re- 
duction  of  undue  arterial  tone  and  the  amelioration  of  the  general 
health  of  the  patient. 

Tonics,  in  the  form  of  iron,  arsenic,  etc.,  are  useful  in  some  cases, 
while  in  others  nerve  sedatives,  such  as  the  bromides,  belladonna,  or 
valerianate  of  zinc,  etc.,  are  indicated. 

The  hygienic  and  dietetic  measures  mentioned  in  the  account  of 
the  treatment  of  true  angina  are  of  equal  service  in  the  treatment  of 
the  functional  forms  of  the  disease.  In  both  the  organic  and 
functional  varieties  of  the  disorder  a  period  of  rest  must  be  strictly 
enforced  after  the  occurrence  of  a  paroxysm. 


CHAPTER   XXIV 

FUNCTIONAL    DISORDERS   OF   THE 
HEART 


Definition — Etiology — Pathogenesis — Section  I.  Cardiac  Pain  ;  Local  and  Re- 
ferred— Section  II.  Palpitation ;  Definition ;  Causation ;  Features  of  Paroxysm 
— Section  III.  Cardiac  Asthenia — Section  IV.  Alterations  in  the  Rhythm  of 
the  Heart's  Action ;  Arrhythmia  ;  Intermittence  and  Irregularity — Section 
V.  Alterations  in  the  rate  of  the  Heart's  Action — Section  VI.  Tachycardia 
— Section  VII.  Decrease  in  the  rate  of  the  Heart's  Action — Section  VIII. 
Diagnosis  ;  Prognosis  ;  Treatment. 

The  so-called  "  functional  diseases  "  of  the  heart,  with  very  few,  if 
any,  exceptions,  are  not  diseases  in  the  ordinary  acceptation  of  the 
nosological  significance  of  this  term.  They  are  rather  the  symptoms 
of  disease,  or  of  conditions  producing  disease,  which  lead  as  part  of 
their  manifestation  to  derangement  of  the  nervous  and  often  of  the 
muscular  mechanism  of  the  heart. 

In  other  words,  "  functional  disorders  "  of  the  heart  form  part  of 
many  different  groups  of  symptoms,  which  severally  constitute  "a 
disease  "  properly  so-called. 

A  clear  grasp  of  this  conception  will  go  far  to  dissipate  much  of 
the  difificulty  and  confusion  that  has  grown  up  round  the  subject  of 
functional  affections  of  the  heart. 

Nevertheless,  it  has  been  customary,  and  it  is  no  doubt  convenient, 
to  consider  individually  a  somewhat  miscellaneous  collection  of 
symptoms,  which  have  this  feature  in  common  that  they  are  re- 
ferable to  disturbance,  iri  varying  degrees,  both  of  the  motor  and 
sensory  functions  concerned  in  the  regulation  and  control  of  the 
action  of  the  heart. 

The  adoption  of  this  course  of  procedure  here,  in  the  light  of  the 
explanation  given  above,  ought  not,  therefore,  to  give  rise  to  any 
serious  misunderstanding. 

The  chief  manifestations  of  functional  disturbance  of  the  heart 
will  be,  then,  pain,  palpitation,  and  alterations  in  the  rhythm  and 
rate  of  the  organ, 

322 


FUNCTIONAL  DISORDERS  OF  THE  HEART      323 

A  general  survey  of  the  setiological  and  pathological  conditions 
which  underlie  functional  disorders  of  the  heart  will  precede  the 
detailed  consideration  of  the  individual  symptoms. 


.ETIOLOGY  AND    PATHOLOGY 

The  conditions  under  which  disturbance  of  the  nervous  and 
muscular  mechanisms  concerned  in  the  production  and  regulation 
of  the  beat  of  the  heart  may  arise  are  briefly  as  follow : — 

1.  Cardio-vascular  system. 

(a)  Affections  of  the  cardiac  nerves  and  ganglia. 

Pigmentary,  fatty,  sclerotic,  and  other  changes. 
ip)  Affections  of  the  pericarditwi. 

Pericardial  effusion,  adherent  pericardium. 

(c)  Affections  of  the  myocardimn. 

Inflammatory  lesions,  fatty,  fibroid,  and  other  changes 
of  a  less  obvious  but  not  less  important  kind,  conse- 
quent on  alterations  in  the  nutrition  of  the  muscle 
fibres. 

(d)  Affections  of  the  aorta  and  coronary  vessels. 

Dilatation  and  aneurism  of  the  aorta.  Atheroma  of 
the  aorta  and  coronary  arteries. 

{e)    Vaso-motor  changes  in  the  direction  of  sudden  increase  or 
decrease  of  arterial  tofie^ 

2.  Nervous  system. — Fright,  grief,  shock,  and  depressing  emotions 
of  all  kinds  are  prolific  sources  of  cardiac  disturbance.  Scarcely 
less  important  causes  comprise  nervous  exhaustion  from  overwork, 
worry,  anxiety,  want  of  sleep,  etc.     Neurasthenia  and  hysteria. 

Again,  apoplexy,  concussion  of  the  brain,  epilepsy,  cerebral 
tumours,  etc.,  are  concerned  in  the  production  of  cardiac  irregu- 
larity. 

Among  other  causes  are  lesions  of  the  medulla  and  spinal  cord 
(locomotor  ataxy),  mania,  melancholia,  general  paralysis  of  the 
insane. 

Ex-ophthalmic  goitre  may  for  the  sake  of  convenience  be  included 
under  this  head. 

3.  Alimentary  system. — Flatulent  dyspepsia  is  a  potent  cause  of 
functional  disturbance  of  the  heart's  action.  Other  conditions  are 
diseases  of  the  stomach  and  liver,  jaundice,  constipation,  etc. 

4.  Respiratory  system. — Emphysema,  the  early  stages  of  pul- 
monary tuberculosis  and  so  forth,  are  sometimes  found  in  association 
with  functional  disease  of  the  heart. 


324  DISEASES   OF   THE    HEART 

5.  Genito-urinary  system. — Inflammatory  affections  of  the  kid- 
neys and  uremia.  Uterine  and  ovarian  disorders.  Masturbation 
and  sexual  excesses. 

6.  Constitutional  and  febrile  disorders. — Anaemia,  chlorosis, 
gout,  rheumatism,  and  diabetes.  The  acute  infectious  fevers,  as  for 
instance,  diphtheria,  influenza,  etc.  In  convalescence  from  acute 
fevers,  such  as  enteric  fever,  pneumonia,  etc. 

7.  Toxic  influences. — The  abuse  of  tea,  coffee,  alcohol,  and 
tobacco.     In  poisoning  by  lead,  digitalis,  belladonna,  aconite,  etc. 

8.  Hygienic,  dietetic,  and  other  influences. — Unhealthy  hygienic 
surroundings,  insufficient  or  unwholesome  food,  and  sedentary 
occupations  are  predisposing  causes  of  irregular  cardiac  action. 
Over-feeding  is  no  whit  less  important  as  a  cause  of  functional 
disturbance  of  the  heart.  Prolonged  muscular  effort,  or  occasional 
bursts  of  severe  exertion,  more  especially  when  made  in  conjunction 
with  mental  excitement  and  insufficient  food,  are  a  fertile  source  of 
functional  disorders  of  the  heart. 

Nervous  disturbance  of  the  heart's  action  is  more  common  among 
women  than  men,  and  is  particularly  apt  to  arise  at  the  time  of 
puberty,  and  during  the  climacteric  period. 

It  will  appear,  therefore,  that  disturbance  of  the  neuro-muscular 
mechanism  of  the  heart  may  be  due  to  a  large  variety  of  conditions, 
which,  however,  can  operate  in  three  directions  only,  viz.  (i)  centrally, 
(2)  locally,  and  (3)  reflexl}-. 

The  nervous  machinery  concerned  in  the  regulation  of  the  beat 
of  the  heart  is  the  cardio-inhibitory  centre  in  the  medulla,  the  tenth 
nerves  or  vagi  which  convey  "  inhibitory "  impulses,  and  the 
sympathetic  nerves  which  transmit  "augmentor"  or  "accelerating" 
impulses  to  the  heart. 

The  local  mechanism  comprises  nervous  and  muscular  parts, 
through  which  the  rate  and  rhythm  of  the  cardiac  beat  may  be 
variously  modified. 

Finally,  in  considering  the  influences  which  regulate  or  modify  the 
beat  of  the  heart,  it  is  necessary  to  include  the  effect  of  vaso-motor 
changes.  Stated  briefly,  the  relation  of  the  beat  of  the  heart  to 
blood  pressure  is  that  "the  rate  of  the  beat  is  in  inverse  ratio  to  the 
arterial  pressure  "  (Foster).  In  other  words,  a  rise  of  blood  pressure 
is  accompanied  by  a  decrease,  while  a  fall  of  blood  pressure  is 
attended  by  an  increase  in  the  rate  of  the  heart  beat.  This  circum- 
stance partly  accounts,  no  doubt,  for  the  acceleration  of  the  heart  in 
fevers  and  other  conditions. 

In  health  the  rate  and  rhythm  of  the  heart  vary  within  wide 
limits  under  the  influence  of  the  fluctuations  of  ordinary  blood 
pressure,  which  through  the  administration  of  the  central  nervous 
system  is  regulated  in  accordance  with  the  ever-varying  needs  of  the 
organism. 


FUNCTIONAL  DISORDERS  OF  THE  HEART      325 

Normally  the  action  of  the  heart  is  in  all  probability  kept  under 
continuous  control  by  impulses  passing  along  the  vagi  from  the 
cardio-inhibitory  centre.  Acceleration  of  the  heart,  therefore,  may 
be  due  either  to  relative  or  absolute  loss  of  vagus  control.  Thus 
stimulation  of  the  sympathetic  nerves  may  give  rise  to  im- 
pulses which  overpower  the  normal-  action  of  the  cardio-inhibitory 
mechanism,  or  the  function  of  the  vagi  may  be  more  or  less  in 
abeyance. 

On  the  other  hand,  stimulation  of  the  vagi  either  locally  or 
through  the  cardio-inhibitory  centre  will  lead  to  slowing  of  the 
heart. 

Furthermore,  since  in  disease  loss  of  functional  activity  proceeds 
pari  passu  with  the  degree  of  its  specialization,  the  controlling 
machinery  of  the  heart  will  fail  before  the  accelerating  mechanism, 
and  herein  may  lie  part  of  the  explanation  of  the  rapid  cardiac 
action  in  cases  of  fever,  poisoning,  and  so  forth. 

Alterations  in  the  rate  and  rhythm  of  the  heart  may  also  depend 
on  interference  with  the  nutrition  of  the  organ,  or  on  the  direct 
action  on  the  muscular  substance  of  imperfectly  oxidized  products 
of  metabolism,  or  of  poisons  circulating  in  the  blood  (cf.  irritable 
heart,  fatty  heart,  gout,  rheumatism,  jaundice,  etc.). 

Again,  local  or  reflex  excitation  of  the  cardio-inhibitory,  vaso- 
motor, and  cardio-augmentor  (?)  centres  must  be  a  prolific  source  of 
disturbance  of  the  cardiac  action. 

Under  normal  conditions  the  harmonious  co-operation  of  these 
centres,  under  the  influence  of  local  and  reflex  stimuli,  regulates  the 
blood  pressure,  and  hence  the  blood  flow  in  accordance  with  the 
demands  of  the  system  by  alterations  in  the  rate  and  rhythm  of 
the  heart.  It  is  not  surprising,  therefore,  that  under  conditions 
of  disease  this  complex  mechanism  becomes  deranged  with  corre- 
sponding modifications  in  the  rate  and  rhythm  of  the  heart. 

Palpitation  is  an  instance  of  such  abnormal  action.  Here,  as 
the  result  of  emotion  or  other  mental  disturbance,  the  action  of 
the  cardio-inhibitory  centre  itself  is  suddenly  inhibited,  or  there 
is  a  sudden  increase  of  the  augmenting  impulses  along  the 
sympathetic  nerves  which  overpowers  the  normal  controlling 
mechanism  of  the  heart,  or  possibly  there  is  a  combination  of 
these  conditions.  Nor  does  this  exhaust  the  possible  methods  by 
which  the  attack  may  be  explained,  for  emotional  disturbance  leads 
also  to  sudden  vaso-motor  changes,  either  in  the  direction  of  arterial 
constriction  or  relaxation,  and  in  this  way  may  give  rise  to  the 
phenomena  of  the  paroxysm. 

Take  again  the  case  of  fevers,  which  by  producing  alterations  in 
the  quantity  and  quality  of  the  blood  give  rise  not  only  to  a  fall 
of  blood  pressure  and  stimulation  of  the  cardiac  accelerating 
mechanism,  but  also  to  more  or  less  direct  poisoning  of  the 
muscular  substance  of  the  heart. 

The  heart,  therefore,  with  respect  to  the  neuro-muscular  machinery 


326  DISEASES   OF  THE    HEART 

concerned  in  the  regulation  of  its  beat,  may  be  attacked  either 
centrally,  locally,  or  reflexly,  as  well  as  through  the  collateral  channel 
of  the  vaso-motor  mechanism. 

It  will  thus  appear  how  complex  may  be  the  operation  of  the 
conditions  which  give  rise  to  alterations  in  the  rate  and  rhythm 
of  the  heart. 

The  mode  of  origin  of  the  pain  and  other  distressing  sensations 
which  may  accompany  the  symptoms  comprised  under  the  term 
"  functional  disorders  of  the  heart "  is  not  fully  understood. 

Normally  the  cardiac  afferent  impulses  which  travel  along  the  vagi 
and  sympathetic  nerves  do  not  give  rise  to  any  perceptible  im- 
pressions ;  in  other  words,  we  are  ordinarily  unconscious  of  the 
action  of  the  heart. 

Now,  an  increase  in  the  intensity  of  the  peripheral  stimuli,  and 
hence  of  the  cardiac  afferent  impulses,  or  an  irritable  condition 
of  the  nervous  structures  engaged  in  transmitting  and  receiving 
these  impulses,  might  give  rise  to  sensation  of  a  more  or  less 
painful  nature. 

Thus  in  organic  disease  of  the  heart,  whether  valvular  or  mural, 
the  increase  of  intra-cardiac  pressure,  and  the  accompanying  dis- 
tension of  one  or  other  of  the  chambers  of  the  organ,  must  give 
rise  to  undue  stretching  and  compression  of  the  peripheral  cardiac 
nerves,  and  in  this  way  to  irritation  of  these  structures  which  may 
be  felt  as  pain.  Again,  in  conditions  of  nervous  irritability,  which 
must  also  involve  the  cardiac  innervation  (both  central  and 
peripheral),  the  ordinary  afferent  impulses  may  be  sufficient  to 
give  rise  to  painful  impressions.  Furthermore,  if  an  irritable 
condition  of  the  cardiac  nerves  (both  central  and  peripheral) 
be  associated  with  an  increase  in  the  intensity  of  the  peripheral 
stimuli  a  fortiori,  a  still  greater  effect  would  be  produced,  and 
the  painful  impressions  may  then  extend  and  overflow  to  other 
nerves  in  connection  with  the  cardiac  innervation,  as  in  the  case 
of  angina  pectoris,  and  other  organic  affections  of  the  heart. 

The  pain,  therefore,  that  is  occasioned  by  diseases  of  the  heart 
may  be  either  local  or  referred. 

According  to  Head,  local  pain  is  limited  strictly  to  the  precordial 
area,  and  is  not  accompanied  by  superficial  tenderness.  It  is,  how- 
ever, usually  attended  by  deep  tenderness,  which  is  increased  by 
pressure  in  direct  ratio  to  the  force  applied.  Further,  local  pain 
is  not  accompanied  by  that  form  of  headache  which  is  associated 
with  tenderness  of  the  scalp. 

Referred  pain,  on  the  other  hand,  is  distributed  over  more  or  less 
well-defined  areas  situated  both  on  the  anterior  and  posterior  aspects 
of  the  chest  wall,  and  also  in  other  parts  of  the  body,  and  is 
accompanied  by  superficial  tenderness,  which  is  usually  relieved 
by  pressure. 

Referred  pain  is  hkewise  commonly  attended  by  headache  and 
superficial  tenderness  of  the  scalp  in  the  supra-orbital  and  temporal 


FUNCTIONAL  DISORDERS  OF  THE  HEART      327 

regions.     For   further   information   on   this   subject   the   reader   is 
referred  to  Dr.  Head's  paper  in  Brain  (Ixxiv.  and  Ixxv.). 

The  following  account  of  the  symptoms  of  functional  diseases  of 
the  heart  do  not  apply  to  the  similar  manifestations  associated  with 
organic  lesions  of  the  organ,  for  the  reason  that  these  have  already 
been  considered  in  other  sections  of  this  work. 


SECTION    I 

CARDIAC   PAIN 

Local  cardiac  pain  is  probably  more  often  complained  of  in 
connection  with  functional  than  with  organic  disease  of  the  heart. 

The  pain  is  most  commonly  felt  over  the  region  of  the  apex 
beat,  less  frequently  in  the  third  or  fourth  left  intercostal  space ; 
but  it  may  be  experienced  over  any  portion  of  the  prsecordial 
region.  It  is  usually  possible  to  evoke  a  greater  or  less  degree 
of  tenderness  by  pressure  over  the  seat  of  pain.  Care  must, 
however,  be  taken  not  to  confound  true  local  pain  with  referred 
pain,  which  is  also  frequently  experienced  over  the  prsecordial 
region  in  cases  of  functional  disease  of  the  heart. 

Cardialgia  is  apt  to  occur  in  paroxysms,  and  is  very  commonly 
associated  with  breathlessness,  or  oppression  of  breathing.  The 
pain  is  variously  described ;  at  one  time  it  is  tearing,  cutting, 
stabbing,  or  burning  in  character ;  at  another  it  is  a  dull,  heavy, 
persistent  ache.  The  suffering  of  the  patient  is  often  very  greatly 
intensified  by  the  fear  that  he  or  (more  commonly)  she  is  the 
subject  of  heart  disease. 

The  pain  is  generally  increased  by  fatigue  or  emotional  disturb- 
ance, and  sometimes  by  exertion ;  on  the  other  hand,  moderate 
exercise  may  bring  relief  to  the  pain.  Attacks  of  palpitation, 
when  they  occur,  usually  aggravate  the  suffering  of  the  patient. 

Local  cardiac  pain  may  arise  in  various  ways.  Thus  it  may 
depend  on  intrinsic  causes,  such  as  have  already  been  considered. 
It  may  also  .be  due  to  extrinsic  conditions,  as,  for  instance,  the 
direct  pressure  exerted  on  the  heart  by  distension  of  the  stomach 
or  abdomen,  or  by  fluid  or  air  in  the  pleural  cavity. 

Again,  reflex  disturbance  of  the  heart,  often  associated  with  pain 
in  the  prsecordial  area,  is  very  commonly  produced  by  sudden 
emotion,  or  by  prolonged  grief  or  anxiety. 

The  pain  over  the  heart  that  is  so  frequently  found  in  connection 
with  conditions  of  nervous  strain  or  exhaustion,  digestive  derange- 
ments, and  uterine  or  ovarian  disorders  is  also  due  to  reflex 
disturbance  of  the  organ. 


328  DISEASES    OF   THE    HEART 


SECTION    II 
PALPITATION 

Palpitation  is  essentially  a  paroxysmal  affection  characterized  by 
frequent,  forcible,  and  oftentimes  irregular  action  of  the  heart, 
which  is  perceptible  to  the  sufferer. 

A  variety  of  the  disorder,  sometimes  termed  false  palpitation, 
is  distinguished  by  a  distressing  subjective  sensation  of  cardiac 
action,  although  on  physical  examination  no  appreciable  alteration 
in  the  rate  or  rhythm  of  the  heart  can  be  detected.  On  the  other 
hand,  the  most  extreme  derangement  of  the  heart's  action,  both 
as  regards  rate  and  rhythm,  may  be  found  without  any  consciousness 
of  the  disturbance. 

The  distinctive  feature  of  palpitation  is,  therefore,  a  more  or  less 
distressing  perception  of  the  beating  of  the  heart. 

The  predisposing  causes  of  palpitation,  apart  from  organic 
disease  of  the  heart,  are  loss  of  tone  or  undue  excitability  of  the 
nervous  system,  neurasthenia,  hysteria,  mental  or  physical  ex- 
haustion, general  loss  of  tone,  as,  for  instance,  is  observed  after 
the  acute  fevers  and  other  exhausting  diseases,  masturbation  and 
sexual  excesses,  and  certain  disordered  conditions  of  the  blood, 
to  wit,  lithsemia,  aneemia,  and  the  like.  Palpitation  is  more 
common  among  women  than  men,  and  is  especially  apt  to  arise 
during  periods  of  nervous  stress  and  excitement,  such,  for  instance, 
as  are  observed  at  the  time  of  puberty  and  the  climacteric. 

Among  the  chief  exciting  causes  of  palpitation  may  be  mentioned 
sudden  emotion,  shock,  grief,  fright,  etc.,  violent  exercise,  digestive 
disturbances,  especially  when  attended  by  flatulence,  uterine  and 
ovarian  disorders. 

The  abuse  of  alcohol,  tobacco,  tea,  coffee,  etc.,  is  also  a  common 
exciting  cause  of  palpitation. 

A  brief  reference  must  be  made  here  to  the  condition  described 
by  Da  Costa  under  the  title  of  irritable  heart. 

According  to  AUbutt  it  is  possible  to  distinguish  two  classes 
of  this  disorder ;  the  one,  a  curable  affection  occurring  for  the  most 
part  in  young  men ;  the  other,  frequently  an  incurable  condition, 
observed  principally  among  soldiers  (hence  called  by  Allbutt  "the 
soldier's  heart "). 

The  irritable  heart  of  young  people  is  found  chiefly  in  ill- 
developed,  nervous,  and  dyspeptic  subjects,  and  is  the  product 
of  occasional  bursts  of  more  or  less  severe  muscular  exertion  in 
conjunction  with  irregular  habits  with  respect  to  the  taking  of  food 
and  the  use  of  alcohol,  tea,  coffee,  tobacco,  and  the  like. 

The  symptoms  qf   this  form  of   irritable  heart  are   palpitation 


FUNCTIONAL  DISORDERS  OF  THE  HEART     329 

and  more  or  less  constant  praecordial  uneasiness  or  pain  with  easily 
excited  dyspnoea.  Physical  examination  of  the  chest  reveals 
excited  action  of  the  heart,  sometimes  in  association  with  a  little 
dilatation  of  the  organ,  and  occasionally  with  slight  hypertrophy. 

The  blood  pressure  in  these  cases  is  nearly  always  low. 

"The  soldier's  heart"  is  usually  observed  among  raw  recruits, 
and  is  due  to  cardiac  overstrain  consequent  on  the  severe  muscular 
exertion  entailed  by  driUing,  forced  marches,  etc.,  in  conjunction 
with  mental  excitement  and  insufficient  training,  or  with  an 
enfeebled  state  of  the  muscular  tissues  following  attacks  of  fever 
or  diarrhoea,  insufficient  food,  and  the  abuse  of  alcohol  and 
tobacco. 

The  symptoms  of  this  variety  of  irritable  heart  are  palpitation, 
cardiac  pain,  dyspnoea  on  exertion,  and  a  tendency  to  the  pro- 
duction of  a  great  increase  in  the  pulse  rate  on  very  slight 
provocation. 

The  heart  is  usually  somewhat  enlarged,  more  in  the  direction 
of  dilatation  than  of  hypertrophy,  while  the  cardiac  sounds  show 
but  little  deviation  from  the  normal. 

The  pulse  rate  is  increased,  and  the  blood  pressure  is  low. 

This  condition  of  irritable  heart  is  of  importance  from  the  fact 
that  it  eventually  gives  rise  to  hypertrophy  of  the  organ,  and 
possibly,  in  some  instances,  to  valvular  disease.  Dilatation  of  the 
heart  ultimately  supervenes  with  its  effects. 

The  ordinary  forms  of  neurotic  palpitation  seldom,  if  ever,  give 
rise  to  organic  disease  of  the  heart. 

An  attack  of  palpitation  usually  commences  abruptly,  sometimes 
with,  but  perhaps  more  commonly  without,  an  obvious  exciting 
cause.  It  not  infrequently  happens  that  the  patient  is  waked  up 
from  sleep  by  the  tumultuous  beating  of  the  heart.  The  excited 
and  violent  pulsation  of  the  organ  is  often  attended  by  more  or 
less  precordial  uneasiness  or  discomfort,  seldom  amounting  to 
actual  pain.  A  distressing  feeling  of  choking  or  suffocation,  accom- 
panied by  oppression  of  the  breathing,  is  frequently  experienced. 
Violent  throbbing  of  the  arteries,  noises  in  the  ears,  giddiness, 
faintness,  and  a  sense  of  fulness  in  the  head  are  not  uncommon 
features  of  the  paroxysm. 

The  face  may  be  pale  or  flushed,  and  bedewed  with  sweat,  while 
the  features  are  frequently  expressive  of  anxiety  or  alarm. 

The  attack  may  last  a  few  minutes,  or  may  extend  over  several 
hours.  It  usually  ceases  abruptly  with  a  kind  of  shock,  but  in  some 
instances  a  more  gradual  subsidence  of  the  symptoms  is  observed. 
The  termination  of  the  paroxysm  is  sometimes  marked  by  the 
passage  of  a  large  quantity  of  pale-coloured  urine.  An  attack  of 
palpitation  is  followed  by  a  greater  or  less  degree  of  exhaustion. 

An  examination  of  the  heart,  during  a  paroxysm,  usually  shows 
an  increase  in  the  area  of  visible  cardiac  pulsation. 

Palpation  may  discover  forcible  action  of  the  heart,   but  more 


330  DISEASES   OF   THE    HEART 

often  the  impulse  of  the  organ  is  felt  as  a  slap  or  tap,  and  in  cases 
of  extremely  rapid  cardiac  action,  as  a  mere  vibration  only. 

The  area  of  cardiac  dulness  is  not  increased. 

The  sounds  at  the  apex  are  usually  short  and  loud,  while  at  the 
base  the  second  sound  may  be  accentuated,  but  more  commonly  it 
is  weak.  Approximation  of  the  sounds  is  the  rule,  but  when  the 
heart  is  acting  very  rapidly,  the  two  sounds  become  equidistant  in 
their  time  relations,  and  more  or  less  similar  in  character,  so  that 
the  foetal  heart  beat  is  very  closely  simulated. 

Murmurs  are  not  infrequently  audible  during  an  attack  of  palpita- 
tion. They  are  systolic  in  time,  and  are  heard  most  commonly 
at  the  apex  of  the  heart.  The  method  of  production  of  these 
temporary  murmurs  is  uncertain ;  while  some,  no  doubt,  are  of 
h^mic,  or  cardio-pulmonary  origin,  others  are,  in  all  probability, 
due  to  relative  incompetence  of  the  mitral  valve. 

The  pulse  reflects  the  excited  condition  of  the  heart. 

Irregularity  of  the  pulse  is,  in  some  instances,  due  to  the  failure 
of  the  heart  to  transmit  the  pulse  wave  as  far  as  the  radial  artery. 
The  tension  of  the  pulse  may  be  high  or  lov/,  under  the  influence 
of  the  vaso  -  motor  changes  which  are  so  commonly  found  in 
association  with  attacks  of  palpitation. 


SECTION    III 

CARDIAC  ASTHENIA 

Under  the  title  of  "cardiac  asthenia,"  Da  Costa  has  compara- 
tively recently  given  an  account  of  a  functional  disorder  of  the 
heart  which  he  distinguishes  from  irritable  heart,  and  which,  in  all 
probability,  has,  up  to  the  present,  been  included  under  the  some- 
what indefinite  description  of  "weak  heart."  A  patient  of  the 
author's,  who  probably  suffered  from  this  variety  of  functional 
disorder,  complained  of  a  "  tired  heart,"  a  description  which  more 
or  less  exactly  fits  the  affection  in  question. 

The  malady  may  occur  at  almost  any  age,  in  either  sex,  and  is 
especially  apt  to  attack  persons  who  have  been  exposed  to  nervous 
strain. 

The  incidence  of  the  disorder  is  always  sudden,  and  is  accom- 
panied by  a  greater  or  less  degree  of  prostration,  manifested  by 
muscular  feebleness,  frequent  sighing  and  yawning,  and  a  tendency 
to  faint  on  the  least  exertion. 

There  is  no  shortness  of  breath,  or  other  disturbance  of  respira- 
tion. A  general  feeling  of  chilliness  may  be  experienced,  and  the 
temperature  is  subnormal. 

Sleeplessness  is  not  an  uncommon  feature  of  the  disorder. 

A  sense  of  prsecordial  discomfort  more  distressing  than  actual 


FUNCTIONAL  DISORDERS  OF  THE  HEART      331 

pain  is  experienced,  and  the  patient  is  hardly  ever  without  a  sort  of 
semi-consciousness  of  the  heart's  action. 

Examination  of  the  heart  demonstrates  a  feeble,  possibly  slightly 
diffused  impulse.  The  percussion  dulness  is  normal.  At  the  apex 
the  sounds  of  the  heart  are  short  and  feeble ;  the  second  sound  at 
the  base  is  not  accentuated. 

In  some  instances  the  action  of  the  heart  is  irregular. 

Murmurs,  more  especially  at  the  apex,  may  be  present. 

The  pulse  is  small,  and  of  extremely  low  tension. 

There  are  no  signs  of  circulatory  disturbance  beyond  those 
already  mentioned. 

The  disorder  generally  persists  for  some  months,  and  recovery, 
though  usually  complete,  is  very  slow. 


SECTION    IV 

ALTERATIONS   IN   THE   RHYTHM   OF   THE 
HEART'S   ACTION 

ARRHYTHMIA 

The  meaning  of  the  word  "  rhythm  "  as  applied  to  the  action  of 
the  heart  is  the  numerical  harmony  or  proportion  of  the  beats  of 
the  organ. 

Alterations  in  the  rhythm  of  the  heart's  action  may  take  place  in 
two  directions,  i.e.  (i)  by  the  occasional  omission  of  a  beat,  and 
(2)  by  the  appearance  of  beats  at  unequal  intervals  of  time,  which 
practically  necessitates  inequalities  in  the  force  and  volume  of  the 
beats. 

These  deviations  from  the  normal  rhythm  are  known  respectively 
as  "  intermittence  "  and  "  irregularity  "  of  the  heart's  action. 

Either  abnormality  may  occur  independently,  but  in  a  large 
number  of  cases  they  are  combined.  Regular  irregularity  of  the 
cardiac  rhythm  is  sometimes  described  under  the  term  "allor- 
rhythmia." 

Intermittence  of  the  heart's  action  may  occur  at  regular  or 
irregular  intervals.  Intermittence  of  the  pulse  does  not  necessarily 
mean  the  dropping  of  a  cardiac  beat,  since  the  ventricular  con- 
traction, though  audible,  may  not  be  sufificiently  powerful  to  propel 
the  pulse  wave  as  far  as  the  radial  artery. 

Intermittence  of  the  heart's  action  is  for  the  most  part  a  sign  of 
trivial  significance.  It  is,  however,  sometimes  found  in  association 
with  fatty  degeneration  of  the  cardiac  wall,  and  may  then,  if 
habitual,  be  of  grave  import.  Its  occurrence,  too,  in  connection 
with  cerebral  disorders  and  acute  affections  of  the  lungs  is  also  of 
serious  augury. 


332  DISEASES   OF   THE   HEART 

Irregularity  of  the  heart's  action  may  be  incidental  or  more  or  less 
constant.  It  is  occasionally  of  little  or  no  importance,  but  it  is, 
generally  speaking,  always  of  much  graver  significance  than  inter- 
mittence,  more  especially  in  connection  with  organic  disease  of  the 
heart.  A  combination  of  intermittence  and  irregularity  of  the 
cardiac  action  under  these  conditions  increases  the  gravity  of  the 
prognosis.  As  a  rule  irregularity  of  the  heart's  action  is  more 
serious  when  habitual  than  when  occasional. 

The  following  disturbances  of  the  cardiac  rhythm  are  observed 
in  addition  to  those  already  mentioned,  as  the  result  of  the  operation 
of  one  or  both  of  the  factors  concerned  in  the  production  of 
arrhythmia. 


FIG.  42.       BIGEMINAL    PULSE    TRACING 


>r^ 


FIG.   43.       TRIGEMINAL   PULSE   TRACING 

The  alternate  heart  beat  corresponding  with  the  pulsus  alternans 
is  produced  by  repeated  and  successive  strong  and  weak  ventricular 
contractions. 

A  duplicate  or  triplicate  arrangement  of  the  cardiac  action  may 
be  observed,  so  that  groups  of  two  or  three  beats  occur  with  a  pause 
between  each  group. 

The  pulsus  bigeminus  and  pulsus  trigeminus  are  respectively  the 
peripheral  expression  of  these  two  forms  of  cardiac  arrhythmia.  In 
the  pulsus  bigeminus  the  second  beat  is  usually  the  weaker  of  the 
two.  The  weakness  of  the  second  beat  may  be  carried  to  the  point 
of  extinction,  so  that  two  beats  of  the  heart  occur  to  one  of  the 
pulse. 

These  varieties  of  arrhythmia  occur  most  commonly  in  mitral 
stenosis,  more  especially  when  under  the  influence  of  digitalis. 


FUNCTIONAL  DISORDERS  OF  THE  HEART     333 

The  alteration  in  the  rhythm  of  the  heart's  action  which  gives 
rise  to  the  pulsus  paradoxus  is  an  illustration  of  the  influence  of 
respiration  on  a  weak  or  hampered  left  ventricle. 

The  most  extreme  disturbance  of  the  cardiac  rhythm  is  observed 
in  the  condition  known  as  delirium  cordis. 

The  alterations  in  the  rhythm  of  the  heart's  action  associated  with 
approximation,  spacing  and  reduplication  of  the  cardiac  sounds, 
together  with  their  significance,  have  been  considered  in  previous 
sections  (see  pp.  50  and  51). 

The  chief  causes  of  disturbance  of  the  cardiac  rhythm,  exclusive 
of  structural  lesions  of  the  heart,  are  functional  and  occasionally 
organic  affections  of  the  brain,  the  acute  specific  fevers,  and  acute 
disease  of  all  kinds,  but  more  especially  of  the  lungs  and  kidneys, 
flatulent  dyspepsia,  and  reflex  irritation  from  gastro-intestinal  and 
hepatic  derangements,  sexual  irregularities,  and  the  like. 

Arrhythmia  is  also  commonly  due  to  the  abuse  of  tobacco,  tea, 
alcohol,  etc.,  and  to  the  action  of  certain  drugs,  notably  of  digitalis, 
belladonna,  and  aconite. 

Gout  and  allied  disorders  are  also  productive  of  intermittent  and 
irregular  action  of  the  heart. 

It  frequently  happens  that  cardiac  intermittence  or  irregularity  lie 
outside  the  sphere  of  consciousness,  and  this  is  especially  likely 
to  be  the  case  when  the  disturbance  of  rhythm  is  associated  with 
organic  disease  of  the  heart,  and  is  therefore  more  or  less  constant. 
On  the  other  hand,  intermittent  action  of  the  heart  is  not  un- 
commonly attended  by  a  fluttering  or  sinking  sensation  in  the 
precordial  area,  followed  by  a  thump  or  bump  as  the  cardiac 
action  is  resumed  with  a  somewhat  more  powerful  contraction  than 
usual. 

Apart  from  palpitation,  irregular  action  of  the  heart  is  rarely 
perceptible  to  the  patient.  It  is  said  that  disturbance  of  the  cardiac 
rhythm  is  of  less  moment  when  attended  by  subjective  sensations 
than  when  it  is  not. 

Physical  examination  of  the  heart  in  cases  of  cardiac  intermittence 
sometimes  shows  that  the  dropping  of  the  beat  is  apparent  rather 
than  real,  since  there  is  evidence  that  the  ventricular  contraction 
occurs  but  is  not  sufficiently  powerful  to  transmit  the  pulse  wave  as 
far  as  the  wrist. 

In  some  instances,  however,  a  real  omission  of  the  beat  takes 
place,  so  far  as  the  absence  of  auscultatory  and  other  physical  signs 
can  demonstrate  this  occurrence. 


334  DISEASES    OF   THE    HEART 

SECTION  V 

ALTERATIONS   IN   THE   RATE   OF   THE   HEART'S 

ACTION 

Alterations  in  the  rate  of  the  heart's  action  lead  either  to  an 
increase  or  to  a  decrease  of  its  frequency,  and  these  are  the  aspects 
under  which  the  subject  will  be  considered. 

I.  Increase  in  the  Rate  of  the  Heart's  Action 

Increased  frequency  of  the  heart's  action,  which  may  amount 
to  eighty,  ninety,  or  even  one  hundred  beats  per  minute,  is  a  normal 
phenomenon  in  some  individuals.  Otherwise  the  causes  of  an  increase 
in  the  rate  of  the  heart's  action  are  practically  any  of  the  conditions 
that  were  enumerated  under  the  heading  of  "setiology"  at  the  begin- 
ning of  this  chapter.  Palpitation  and  rapid  heart  rate  are  very 
commonly  associated,  but  they  may  and  frequently  do  occur  inde- 
pendently. 

An  increase  in  the  frequency  of  the  heart's  action  is  symptomatic 
of  the  affection  known  as  ex-ophthalmic  goitre,  and  it  is  found 
sooner  or  later  in  almost  all  forms  of  organic  disease  of  the  heart. 
It  is  also  observed  in  connection  with  certain  lesions  of  the  vagus 
nerve  and  medulla  oblongata. 

The  effect  of  an  increase  in  the  rate  of  the  heart's  action  on  the 
time  relations  of  the  various  events  comprising  the  cardiac  cycle 
is  to  shorten  the  diastole.  The  shortening  of  the  diastole  interferes 
with  the  proper  filling  of  the  heart  with  blood,  so  that  not  only 
is  the  output  per  ventricular  contraction  greatly  reduced,  but  also 
the  gross  output  per  unit  of  time  is  not  increased,  and  may  be 
diminished. 

It  is  obvious,  therefore,  that  rapid  action  of  the  heart  does  not 
per  se  add  to  the  work  of  the  organ,  and  herein  may  lie  to  a  large 
extent  the  explanation  of  the  absence  of  cardiac  hypertrophy,  even 
after  long-continued  increase  in  the  rate  of  the  heart's  action. 


SECTION   VI 
TACHYCARDIA 

Paroxysmal  attacks  of  extremely  rapid  cardiac  action,  attended  by 
palpitation  and  more  or  less  prsecordial  discomfort,  are  distinguished 
under  the  title  of  tachycardia,  which  may  possibly  represent  a  true 
neurosis  of  the  heart. 

Tachycardia  is  found  chiefly  among  neurotic  subjects  of  either 
sex,  and  it  may  occur  at  almost  any  age.  In  some  cases  among 
women  the  attacks  have  appeared  for  the  first  time  about  the  period 


FUNCTIONAL  DISORDERS  OF  THE  HEART      335 

of  the  menopause.  An  hereditary  influence  has  been  remarked  in 
occasional  instances. 

The  causation  of  tachycardia  has  not  yet  been  satisfactorily  deter- 
mined. The  attacks,  in  some  instances,  have  appeared  to  depend 
on  emotional  disturbance,  gastric  derangements,  uterine  displace- 
ments, pregnancy,  floating  kidney,  over-exertion,  and  so  forth.  In 
other  cases  the  abuse  of  tobacco,  alcohol,  etc.,  has  appeared  to 
exert  a  causal  influence  in  the  production  of  the  disorder.  In  a 
case  observed  by  the  author,  the  attacks  occurred  apparently  as  a 
sequel  of  acute  rheumatism. 

The  pathogenesis  of  tachycardia  is  equally  uncertain. 

The  rapid  action  of  the  heart  has  been  explained  on  the  supposi- 
tion of  loss  of  vagus  control,  or  of  discharging  lesions  affecting  the 
"  accelerating  "  centres,  or  of  a  combination  of  these  causes.  Lesions 
of  the  cardiac  ganglia  and  vaso-motor  changes  have  also  been  as- 
signed a  share  in  the  causation  of  the  attacks. 

As  a  working  hypothesis  it  may  be  supposed  that  in  cases  of 
tachycardia  there  is  an  unstable  condition  of  the  neuro-muscular 
mechanism  concerned  in  the  regulation  of  the  heart's  action,  which 
would  affect  chiefly  the  controlling  function  of  the  vagi  and  cardio- 
inhibitory  centre  as  well  as  of  the  vaso-motor  centre.  Under  these 
circumstances  reflex  or  centric  irritation  of  the  neuro-muscular 
apparatus  of  the  heart  might,  through  the  accelerating  mechanism, 
be  capable  of  giving  rise  to  the  phenomena  of  the  attacks. 

The  paroxysms  commence  suddenly  with  a  feeling  of  tightness, 
uneasiness,  or  oppression  in  the  praecordial  region,  accompanied 
by  a  more  or  less  distressing  sensation  of  rapid  cardiac  action.  The 
degree  of  discomfort  experienced  varies  greatly  in  different  cases. 
The  pulse  rate  rapidly  runs  up  to  150,  200,  or  even  250  beats  a 
minute.  In  one  of  the  reported  cases  a  pulse  rate  of  over  300 
beats  a  minute  was  counted  (Bristowe). 

The  heart  acts  regularly,  as  a  rule,  throughout  the  attack,  unless 
dilatation  supervenes,  but  the  pulse  may  become  irregular  owing  to 
the  failure  of  some  of  the  beats  to  reach  the  wrist. 

The  duration  of  the  paroxysm  varies  greatly.  It  may  continue 
for  a  few  hours  or  a  few  days,  and,  it  is  stated,  that  in  exceptional 
instances  it  has  persisted  for  weeks. 

As  a  rule  the  attack  ceases  abruptly,  and  is  followed  by  more  or 
less  exhaustion.  A  copious  secretion  of  urine  may  accompany  the 
terminal  stages  of  the  paroxysm. 

The  attacks  may  recur  at  intervals  of  a  few  hours,  days,  or  weeks, 
or,  as  is  not  infrequently  the  case,  the  period  of  immunity  extends 
into  months  or  even  years. 

A  physical  examination  of  the  heart  during  the  attack  usually 
reveals  nothing  abnormal  beyond  the  modification  in  the  rhythm 
of  the  sounds  that  is  always  associated  with  rapid  cardiac  action. 
The  shortening  of  the  diastole  gives  rise  to  the  so-called  foetal  heart 
rhythm,  or  tick-tack  action  of  the  heart. 


336  DISEASES    OF   THE    HEART 

Recovery  is  usually  complete,  provided  the  interval  between  the 
attacks  is  sufficiently  long  to  enable  the  heart  to  recuperate.  In 
some  instances  the  repeated  occurrence  of  the  attacks  at  short 
intervals  exhausts  the  heart,  and  dilatation  then  supervenes  together 
with  its  effects.  Death,  under  these  circumstances,  may  be  due  to 
gradual  failure  of  the  heart  or,  as  is  more  often  the  case,  to  syncope. 


SECTION   VII 
DECREASE  IN  THE  RATE  OF  THE  HEART'S  ACTION 

The  term  "  bradycardia "  or  brachycardia  is  used  to  denote  slow 
action  of  the  heart.     It  has  no  other  significance. 

An  infrequent  action  of  the  heart,  by  which  is  meant  a  rate  below 
fifty  beats  a  minute,  is  a  normal  condition  in  some  individuals. 

A  decrease  in  the  rate  of  the  heart's  action  is  a  physiological 
occurrence  in  parturition  (Osier).  It  is  also  found  in  association 
with  hunger. 

A  slow  action  of  the  heart  is  sometimes  observed  in  connection 
with  fatty  degeneration,  less  often  with  fibroid  disease  of  the  cardiac 
walls.  The  significance  of  the  phenomenon  in  this  respect  is  in- 
creased when  it  occurs  in  association  with  vertigo  and  syncopal 
attacks  (Allbutt). 

A  slow  pulse  does  not  necessarily  imply  an  infrequent  action  of 
the  heart,  since  some  of  the  beats  may  fail  to  reach  the  periphery. 
Deductions  drawn  from  the  pulse  rate  with  respect  to  slowing  of  the 
cardiac  action  should  be  checked,  therefore,  by  an  examination  of 
the  heart. 

Apart  from  the  conditions  mentioned  above,  a  decrease  in  the 
rate  of  the  heart's  action  is  observed  in  association  with — 

1.  A  rise  of  blood  pressure. 

2.  Pain. 

3.  Diseases  of  the  nervous  system. 

Apoplexy,  and   tumours   of    the   brain.     Lesions   of   the 

medulla. 
Diseases  of  the  spinal  cord  {tabes  dorsalis). 
Emotion.     Hysteria,  melancholia,  mania  (occasionally). 

4.  Reflex  irritation  from  gastro-intestinal  derangement,  worms  in 

the  intestinal  tract,  ovarian  and  uterine  disorders,  etc. 

5.  Exhaustion   during   convalescence  from   fever  or   from    over- 

fatigue, sexual  excesses,  etc. 

6.  Toxic  influences,  such  as  by  poisons  associated  with  the  acute 

specific  fevers,  diphtheria,    influenza,  etc.,   or  with  lithsemia 
uraemia,  jaundice,  and  so  forth. 

The  action  of  lead,  tobacco,  digitalis,  and  the  like. 

7.  Stokes  Adams'  disease. 


FUNCTIONAL  DISORDERS  OF  THE  HEART     337 

Slowing  of  the  heart's  action  is  for  the  most  part  effected  by 
direct  or  reflex  stimulation  of  the  central  or  peripheral  connections 
of  the  vagi.  There  is,  however,  both  physiological  and  clinical 
evidence  to  show  that  a  like  result  may  possibly  depend,  to  some 
extent  at  least,  on  direct  stimulation  of  the  cardiac  muscle. 

The  functions  of  the  cardiac  ganglia  are  not  thoroughly  under- 
stood, but  so  far  as  is  known  these  structures  exert  no  influence 
on  the  regulation  of  the  heart's  beat.  Theoretically,  diminished 
functional  activity  of  the  cardiac  accelerating  mechanism  might 
be  attended  by  a  reduction  in  the  rate  of  the  heart's  action,  but 
the  physiological  and  clinical  evidence  bearing  on  this  point  is 
not  sufficiently  convincing  to  admit  of  a  definite  statement. 

Syncope  or  fainting  is  the  only  symptom  that  will  be  considered 
in  connection  with  slowing  of  the  heart's  action.  This  phenomenon, 
which  is  within  the  experience  of  most  people  at  some  period  ot 
their  lives,  is  most  commonly  observed  in  association  with  pain  or 
emotional  disturbance.  As  there  are  all  degrees  of  syncope  between 
death  and  so-called  fainting  attacks,  so  are  there,  no  doubt,  all 
degrees  of  infrequent  cardiac  action  between  complete  arrest  and 
the  reduction  in  rate  necessary  to  produce  symptoms  of  cerebral 
anaemia,  which  is  the  proximate  cause  of  the  phenomena. 

In  an  ordinary  fainting  attack,  due  to  reflex  stimulation  of  the 
vagi  by  pain,  emotion,  etc.,  there  is  probably  a  reduction  in  the 
rate  of  the  heart's  action  in  association  with  ventricular  contractions 
of  so  feeble  a  kind  that  they  are  not  preceptible  within  the  limits  of 
a  physical  examination  of  the  heart. 

There  is  an  additional  factor,  frequently  a  potent  one,  in  the 
production  of  fainting  attacks  of  functional  origin,  viz.  vaso-motor 
disturbance,  which,  by  relaxing  the  vessels  in  the  cutaneous  and 
splanchnic  areas  gives  rise  to  a  fall  of  systemic  blood  pressure. 


STOKES  ADAMS'   DISEASE. 

This  remarkable  symptom-group  or  syndrome  is  characterised  by 
the  occurrence  of  bradycardia  in  association  with  symptoms  that  are 
referable  to  disturbances  of  the  cardio-vascular,  nervous  and  respira- 
tory symptoms.  The  aetiology  and  pathology  of  the  Stokes  Adams' 
syndrome  is  still  obscure,  but  the  conditions  under  which  it  may  be 
observed  are  arranged  by  Osier  in  three  categories,  viz. : — 

1.  Post-febrile  group.  —  In  this  class  the  attacks  follow,  rarely 
accompany,  an  acute  infection  such  as  enteric  fever,  scarlet  fever 
pneumonia,  diphtheria,  influenza,  etc. 

2.  Neurotic  group. — In  this  group  the  syndrome  is  associated  with 
a  gross  lesion  of  the  medulla  or  some  other  portion  of  the  central 
or  peripheral  nervous  apparatus,  or  with  functional  disturbance  of 
the  nervous  system. 

Z 


338  DISEASES    OF   THE    HEART 

3.  Arteriosclerotic  group. — In  this  variety  there  are  found  structural 
changes  in  the  heart  or  vascular  system,  or  in  both.  The  large 
majority  of  the  cases  belong  to  this  group,  and  they  are  observed 
among  men  over  the  age  of  fifty. 

The  central  feature  of  the  Stokes  Adams'  syndrome,  in  its  clinical 
aspect  is  bradycardia,  which  may  be  observed  in  an  acute,  chronic, 
or  intermittent  form  in  different  cases.  The  slowing  of  the  heart 
is  associated  with  vertigo,  syncopal  attacks,  epileptiform  seizures, 
pseudo-apoplexy,  and  respiratory  disorders,  which  will  now  be  briefly 
considered. 

The  bradycardia  or  slowing  of  the  heart  beats,  as  reflected  by  the 
pulse,  may  be  real  or  apparent  only,  inasmuch  as  it  not  infrequently 
happens  that  some  of  the  cardiac  systoles  are  abortive,  and  fail  to 
transmit  the  pulse  wave  as  far  as  the  radial  arteries,  or  even  in  some 
instances  as  far  as  the  carotid  trunks. 

A  temporary  arrest  of  the  heart's  action,  and  vaso-motor  disturb- 
ances in  the  form  of  pallor,  sweating,  etc.,  are  sometimes  observed. 
Vertigo  is  a  very  constant  symptom,  and  may  precede  by  months  or 
years  the  full  development  of  the  syndrome.  Syncope  with  loss  of 
consciousness  is  usually  a  prominent  feature  of  the  disease.  The 
attacks  of  fainting  come  on  suddenly,  and  seldom  last  more  than 
a  minute  or  two,  and  are  apt  to  be  associated  with  convulsive 
seizures  of  an  epileptic  type. 

The  pseudo-apoplectic  phenomena  resemble  the  ordinary  features 
of  an  apoplectic  stroke,  except  that  after  lasting  a  few^  minutes,  con- 
sciousness is  restored  and  the  patient  is  able  to  resume  his  usual 
avocations. 

The  respiratory  disturbances  take  the  form  of  asthmatic  seizures 
and  Cheyne  Stokes'  breathing. 

The  diagnosis  of  Stokes  Adams'  disease  when  fully  developed 
presents  little  or  no  difficulty,  but  in  its  initial  or  slighter  manifesta- 
tions the  sj-ndrome  is  very  easily  overlooked.  The  occurrence  of 
bradycardia  in  association  with  vertigo  should  in  all  cases  suggest 
a  careful  examination  of  the  patient  in  view  of  the  possible  existence 
of  the  symptom  group  under  consideration.  The  prognosis  is  very 
grave,  and  in  the  present  state  of  our  knowledge  of  these  cases  treat- 
ment can  be  symptomatic  only. 


SECTION    VIII 

DIAGNOSIS 

The  diagnosis  of  functional  disorders  of  the  heart  rests  on  the 
presence,  either  alone  or  in  combination,  of  the  symptoms  and  signs 
which  have  been  described.  In  practice  the  chief  difficulty  lies  in 
the  differential  diagnosis  of  the  cause  of  the  cardiac  disturbance. 


FUNCTIONAL   DISORDERS   OF   THE    HEART  339 

more  particularly  with  regard  to  the  exclusion  of  organic  disease  of 
the  heart. 

In  purely  functional  affections  of  the  heart  there  is  an  obvious 
disproportion  between  the  intensity  of  the  subjective  symptoms  and 
the  degree  of  mechanical  disturbance  of  the  circulation.  Moreover, 
palpitation  and  arrhythmia  of  functional  origin  are  sometimes 
relieved  by  exertion,  which  exaggerates  these  symptoms  when  found 
in  association  with  organic  disease  of  the  heart.  This  statement 
does  not  of  course  apply  to  the  palpitation  observed  in  connection 
with  ansemia,  but  in  this  condition  the  cause  of  the  cardiac  disturb- 
ance is  usually  obvious. 

Physical  examination  of  the  heart  in  cases  of  functional  disorder 
rarely  demonstrates  the  presence  of  any  serious  degree  of  cardiac 
enlargement,  though  it  is  not  uncommon  to  find  a  little  dilatation 
of  one  or  both  ventricles.  Moreov-er,  the  character  of  the  sounds 
in  functional  cardiac  affections  is  sometimes  of  service  in  excluding 
organic  disease  of  the  heart. 

Again,  murmurs  heard  in  association  with  functional  disorders  are 
practically  always  systohc  in  time,  and  they  do  not  replace  the  sounds 
of  the  heart  as  in  the  case  of  bruits  due  to  organic  disease  of  the 
organ.  Furthermore,  the  site  of  greatest  audibility  and  the  area 
of  distribution  of  functional  and  organic  apical  systolic  murmurs  do 
not  coincide. 

Apart  from  organic  disease  of  the  heart,  the  differential  diagnosis 
of  the  causes  of  functional  affections  of  the  organ  rests  on  the 
history  of  the  case,  on  the  character  of  the  symptoms,  and  on  the 
causal  indications  furnished  by  the  cardio-vascular  and  other  systems. 

Tachycardia  is  distinguished  from  rapid  action  of  the  heart  due 
to  other  causes  by  its  paroxysmal  character.  An  increase  in  the 
rate  of  the  heart's  action  not  uncommonly  precedes  the  development 
of  the  proptosis  and  th}Toid  enlargement  in  Grave's  disease,  but  in 
this  disorder  the  persistent  acceleration  of  the  pulse  would  suffice  to 
exclude  tachycardia. 

Again,  dilatation  of  the  heart,  mitral  stenosis  in  its  terminal  stages, 
and  bulbar  paralysis  also  give  rise  to  increased  frequency  of  the  pulse ; 
but  in  these  conditions  both  the  rate  and  rhythm  of  the  cardiac 
action  are  more  or  less  persistently  altered,  features  which  are  incon- 
sistent with  tachycardia.  A  paroxysmal  increase  in  the  rate  of  the 
heart's  action  is  sometimes  observ-ed  in  connection  with  the  crises 
of  locomotor  ataxia.  A  correct  diagnosis  seldom  presents  much 
difficulty  in  these  cases,  inasmuch  as  the  attacks  are  associated 
with  disturbance  of  the  cardiac  rhythm  and  with  the  symptoms 
peculiar  to  the  ner\"ous  disorder. 


340  DISEASES   OF   THE    HEART 


PROGNOSIS 

The  prognosis  of  functional  disorders  of  the  heart  is,  on  the 
whole,  favourable  as  regards  the  expectancy  of  life.  The  prospects 
of  recovery,  so  far  as  the  cure  or  prevention  of  the  cardiac  disturb- 
ance is  concerned,  depends,  for  the  most  part,  on  the  extent  to 
which  the  cause  can  be  removed.  In  the  absence  of  a  discoverable 
cause,  and  in  view  of  the  difficulty  which  is  so  often  experienced 
in  excluding  organic  disease  of  the  cardiac  walls,  it  is  advisable, 
before  giving  a  favourable  prognosis  in  a  case  of  functional  disorder 
of  the  heart,  to  make  repeated  and  careful  examinations  of  the 
patient  both  in  the  upright  and  supine  positions. 

The  outlook  with  respect  to  that  variety  of  irritable  heart  known 
as  "soldier's  heart"  (AUbutt)  is  not  good,  inasmuch  as  the  cardiac 
disturbance  leads  ultimately  to  dilatation  and  hypertrophy  of  the 
heart. 

The  prognosis  of  tachycardia  depends  largely  on  the  duration 
of  the  attacks  and  the  frequency  of  their  incidence  (Herringham). 
Long  duration  {i.e.  more  than  four  or  five  days)  and  frequent 
repetition  {i.e.  recurrence  within  a  few  months)  of  the  paroxysms 
involve  more  or  less  cardiac  strain,  which  sooner  or  later  leads  to 
dilatation  of  the  heart  and  its  disastrous  effects.  On  the  other 
hand,  short  attacks  with  protracted  periods  of  immunity  are  com- 
patible with  longevity.  The  prognosis  of  bradycardia  is  the 
prognosis  of  the  cause  of  the  cardiac  disturbance. 


TREATMENT 

The  treatment  of  functional  disorders  of  the  heart  consists  as 
much  in  the  general  management  of  the  patient  as  in  the  employ- 
ment of  drugs.  It  is  obvious  that  in  practice  treatment  should  be 
directed,  in  the  first  instance,  to  the  mitigation  or  relief  of  the 
paroxysms,  and,  secondly,  to  the  prevention  or  removal  of  both 
the  immediate  and  remote  causes  of  the  cardiac  disturbance. 
Nevertheless,  for  descriptive  purposes  it  is  convenient  to  take  the 
second  object  first,  inasmuch  as  certain  general  hygienic,  dietetic, 
and  moral  considerations  are  applicable  in  the  treatment  of  all 
forms  of  functional  disease  of  the  heart,  whereas  special  means  are 
requisite  for  the  relief  of  the  individual  symptoms. 

It  is  of  the  utmost  importance  in  all  cases  of  functional  cardiac 
disorder  to  be  able  to  convince  the  patient  that  there  is  no  disease 
of  the  heart.  While,  on  the  one  hand,  a  careful  investigation  of 
the  condition  of  the  heart  should  be  made  at  the  outset;  on  the 
other,  too  much  attention  should  not  be  directed  to  the  organ 
by   subsequent   examinations.       Moreover,    the    patient's    thoughts 


FUNCTIONAL   DISORDERS   OF   THE    HEART   341 

should  so  far  as  possible  be  diverted  from  his  ailment  by  change 
of  air  and  scenery,  by  cheerful  companionship,  by  the  pursuit  of 
some  wholesome  hobby,  and  by  the  avoidance  of  strain  and  excite- 
ment of  all  kinds. 

A  moderate  amount  of  exercise  in  the  open  air  is  nearly  always 
beneficial,  and  any  outdoor  pursuit  which  does  not  involve  excite- 
ment or  fatigue  may  be  safely  encouraged.  Cold  bathing,  more 
especially  in  the  form  of  shower  baths,  is  frequently  of  service,  but 
should  be  used  with  caution.  Sea  bathing  is  sometimes  attended 
by  the  happiest  results. 

The  adoption  of  an  open-air  life,  and  the  cultivation  of  regular 
habits  with  respect  to  the  taking  of  food,  alcohol,  sleep,  and  exercise, 
is  often  sufficient  to  effect  a  cure. 

Moderation  with  regard  to  the  quantity  of  food,  and  a  common - 
sense  discrimination  with  respect  to  its  quality  are  of  the  first 
importance.  It  is  frequently  advisable  to  altogether  interdict  the 
use  of  tobacco,  alcohol,  tea,  and  coffee. 

Sexual  excesses  are  a  prolific  source  of  functional  disorders  of  the 
heart ;  hence  it  may  become  necessary  to  warn  the  patient  against 
this  form  of  over-indulgence. 

Inasmuch  as  functional  affections  of  the  heart  are  so  frequently 
found  in  association  with  disturbance  of  the  nervous  system,  an 
attempt  should  be  made  to  remove  such  causes  of  mental  strain 
as  overwork,  worry,  anxiety,  and  so  forth.  Hysteria  and  conditions 
of  general  nervous  irritability  or  excitement  may  be  met  by  the  use 
of  bromides,  valerian,  hyoscyamus,  and  other  sedatives. 

Gastro-intestinal  derangements,  which  are  perhaps  the  most 
common  cause  of  functional  disturbance  of  the  heart,  should  be 
corrected  by  careful  dieting,  and  the  exhibition  of  the  remedies 
appropriate  to  the  relief  of  the  particular  kind  of  dyspepsia  that 
obtains.  In  children  the  possible  presence  of  intestinal  worms 
should  not  be  overlooked.  The  bowels  must  be  regulated,  and 
any  source  of  intestinal  irritation,  as,  for  instance,  piles,  should 
receive  attention.  The  correction  of  uterine  displacements  is  some- 
times followed  by  the  disappearance  of  the  cardiac  symptoms. 

Anaemia,  gout  or  lithsemia,  and  other  disordered  conditions  of 
the  blood,  should  receive  appropriate  treatment. 

If  a  careful  and  systematic  investigation  of  the  case  fails  to 
reveal  the  cause  of  the  cardiac  disturbance,  the  drugs  most  likely 
to  be  of  service  are  the  bromides,  salicylates,  or  iodides,  with  or 
without  arsenic,  strychnine,  or  digitalis. 

The  treatment  of  cardiac  pain  depends  for  the  most  part  on 
its  cause.  Digestive  disorders,  uterine  derangements,  emotional 
disturbance,  and  increased  arterio-capillary  resistance  must  be  con- 
trolled and  removed  by  appropriate  means. 

The  application  of  a  belladonna  plaster,  or  of  a  small  blister, 
or,  if  the  pain  be  very  severe,  of  one  or  two  leeches  over  the 
painful  area,   usually  gives  great  relief.     Belladonna  may  also   be 


342  DISEASES    OF   THE    HEART 

given  internally  with  advantage.  In  the  absence  of  a  discoverable 
cause,  or  when  the  pain  resists  other  remedies,  the  administration 
of  one-sixth  of  a  grain  of  barium  chloride  in  pill  form  three  times 
a  day  sometimes  gives  excellent  results. 

An  attack  of  palpitation  can  sometimes  be  relieved  by  exercise 
or  by  the  simple  expedient  of  drawing  a  few  deep  breaths. 

In  general,  the  treatment  of  the  paroxysm  consists  in  rest  in  the 
recumbent  position  and  in  the  use  of  stimulants,  such  as  ether, 
ammonia,  valerian,  ginger  peppermint,  camphor,  and  the  like. 
The  compound  spirits  of  ether,  in  drachm  doses,  is  an  efficient 
remedy  under  these  circumstances.  The  following  prescription  is  an 
example  of  a  very  serviceable  combination  in  the  treatment  of  palpi- 
tation : — 

^  Tincturas  Valerianae  Ammoniatse  5i- 
Tincturas  Lavandulae  Compositse  5ss. 
Spiritus  Vini  Rectificati  Si- 

Aquae  Chloroformi  q.s.   ad.     §ss. 

Fiat  Mistura. 

S.   One  tablespoonful  to  be  taken  every  two  or  three  hours. 

Alcohol,  in  some  warm  vehicle,  is  also  of  service,  but  its 
administration  requires  strict  supervision.  The  vagi  may  also  be 
stimulated  through  the  nasal  mucous  membrane  by  means  of 
smelling-salts,  snuff,  ammonia,  etc.  Hot  or  cold  applications  to 
the  praecordial  region  usually  afford  relief,  but  cold,  in  the  form  of 
an  ice-bag,  must  be  employed  with  caution,  more  especially  if  the 
action  of  the  heart  be  irregular.  In  the  case  of  less  acute  and 
more  protracted  attacks  of  palpitation,  the  various  measures  just 
mentioned  must  be  supplemented  by  treatment  directed  to  the 
more  remote  causes  of  the  cardiac  disturbance. 

With  this  object  the  hygienic  and  dietetic  regulations  which  were 
detailed  at  the  beginning  of  this  section  should  be  put  into  operation. 
The  exhibition  of  nerve  sedatives,  more  especially  of  the  bromide 
of  sodium  or  ammonium,  is  usually  of  service  in  neurotic  cases. 
Belladonna,  given  internally,  or  applied  in  the  form  of  a  plaster 
to  the  prsecordial  region,  is  sometimes  of  service.  The  use  of 
aconite  is  strongly  recommended  by  AUbutt,  but  care  must  be 
observed  in  the  employment  of  this  remedy.  Digitalis  is  seldom 
of  much  benefit,  but  the  administration  of  cactus  grandiflorus,  as 
a  tincture,  is  not  infrequently  attended  by  excellent  results.  Vaso- 
motor disturbances  in  connection  with  palpitation  should  be 
corrected  and  controlled  by  appropriate  treatment.  Tonics  are 
frequently  of  service  in  the  intervals  between  the  attacks. 

The  treatment  of  that  form  of  irritable  heart  which  occurs  in 
young  people  consists  in  the  careful  regulation  of  the  habits  of  the 
patient  as  regards  the  taking  of  food,  exercise,  sleep,  etc.,  and  the  use 
of  such  substances  as  tobacco,  tea,  coffee,  and  alcohol.  Medicinal 
treatment  is  seldom  required.  Complete  rest  for  a  time  is  sometimes 
of  great  benefit  in  these  cases. 


FUNCTIONAL  DISORDERS  OF  THE  HEART  343 

The  treatment  of  so-called  "  soldier's  heart  "  is  very  unsatisfactory. 
Absolute  rest  in  bed,  and  the  administration  of  digitalis  and  aconite 
appear  to  afford  the  best  results.  Cardiac  asthenia  should  be  treated, 
according  to  Da  Costa,  by  rest  in  bed,  followed  by  graduated  shower 
baths,  massage,  and  Swedish  exercises.  The  diet  should  be  nutritious 
and  liberal  as  regards  quantity.  Alcohol  is  also  of  service.  So  far 
as  medicinal  treatment  is  concerned  Da  Costa  strongly  advocates 
the  use  of  strychnine,  and,  failing  this,  of  arsenic  or  of  the  cardiac 
tonics.  Nerve  sedatives  are  occasionally  called  for.  Allbutt  suggests 
that  compression  of  the  abdomen  by  a  properly  fitted  binder  or 
pad  might  be  of  use  in  view  of  the  pathogenesis  of  this  disorder, 
which  he  thinks  may  be  a  dilatation  of  the  vessels  in  the  splanchnic 
area. 

The  treatment  of  arrhythmia  does  not  require  special  considera- 
tion, inasmuch  as  it  turns  on  the  application  of  the  general  principles 
already  indicated.  In  all  cases  treatment  should  be  addressed  to 
the  cause  of  the  cardiac  disturbance,  be  this  digestive  disorder, 
uterine  derangement,  or  the  abuse  of  tea,  alcohol,  tobacco,  coffee, 
etc.  If  the  cause  cannot  be  discovered,  and  provided  the  patient 
suffers  no  inconvenience  from  the  abnormal  cardiac  action,  inter- 
ference by  means  of  drugs  usually  does  more  harm  than  good,  and 
is  therefore  to  be  deprecated. 

Tachycardia  does  not  offer  much  scope  for  treatment,  since  the 
conditions  on  which  the  attacks  depend  are  not  fully  understood. 
The  general  health  of  the  patient  must  be  promoted  by  suitable 
hygienic  and  dietetic  means,  and  any  functional  disturbance  of 
other  organs  which  might  stand  in  causal  relation  to  the  attacks 
should  so  far  as  possible  be  remedied.  DigitaHs  exercises  little  or 
no  influence  on  the  paroxysms,  but  strophanthus  has  occasionally 
appeared  to  do  good.  The  bromides  are  of  service  in  some 
instances,  and  they  may  be  given  in  combination  with  full  doses 
of  belladonna.  The  salicylates  and  iodides  are  also  worthy  of  trial 
w^hen  other  measures  fail. 

Treatment  by  electricity  has  not  fulfilled  expectations,  but  the 
application  of  the  continuous  current  over  the  nerve  trunks  in 
the  neck  has  sometimes  appeared  to  mitigate  the  severity  of  the 
attacks. 

The  treatment  of  bradycardia,  when  this  is  necessary,  should  be 
directed  to  the  cause  of  the  condition. 

In  the  absence  of  organic  disease  of  the  heart,  the  feeling  of 
faintness  which  precedes  the  occurrence  of  actual  syncope  and  loss 
of  consciousness  can  usually  be  relieved  by  making  the  patient  sit 
down  and  bend  forwards  with  the  head  betw^een  the  legs. 

When  fainting  has  occurred  the  patient  should  be  placed  flat  on 
his  back,  with  the  head  at  a  lower  level  than  the  rest  of  the  body. 
The  clothes  round  the  neck,  chest,  and  abdomen  should  be  loosened, 
and  a  current  of  cold  air  allowed  to  play  on  the  skin  wath  the 
object  of  producing  contraction  of  the  superficial  vessels  and  of 
raising  blood  pressure. 


344  DISEASES  OF  THE  HEART 

Reflex  stimulation  of  the  heart  and  respiration  is  accomplished 
by  flicking  the  face  and  chest  with  a  wet  towel  and  by  the  applica- 
tion of  ammonia,  smelling-salts,  and  other  pungent  substances  to 
the  nose.  If  these  measures  fail  to  restore  consciousness,  ammonia, 
ether,  brandy,  or  strychnine  may  be  injected  subcutaneously,  or  per 
rectum. 

When  the  syncopal  attack  is  due  to  hemorrhage  the  patient 
should  be  inverted,  or  the  limbs  bandaged  from  the  feet  upwards, 
with  the  object  of  driving  blood  towards  the  heart  and  brain. 
Meanwhile,  hot  applications  may  be  made  to  the  praecordial 
region. 

In  urgent  cases  artificial  respiration,  galvanization  of  the  phrenic 
nerves,  or  even  transfusion  of  a  saline  solution  may  be  required. 
After  consciousness  is  restored  the  patient  should  remain  in  the 
recumbent  position  until  all  danger  of  a  recurrence  of  the  attack 
has  passed  away. 


INDEX 


Abscess  of  heart,  151,  290,  291 
Accentuation  of  aortic  second   sound, 
48,  205,  270 

of  pulmonic  second  sound,   49, 

175,  187,  272 

Aconite  in  treatment  of  functional  dis- 
orders of  heart,  343 

Adherent  pericardium,  general  account 
of,  129 

Etiology,  general  account  of,  in  cardiac 
disease,  19 

Age,  as  affecting  compensation,  232 
prognosis,  232,  280 

in  aetiology  of  cardiac  disease,  19 

Alcohol,  115,  128,  149,   159,  236,  244, 

282,  287,  289,  293,  303,  320,  342, 
AUbutt,  201,  328,  336,  340,  342 
Ancemia,  20,  21,  24,  63,  146,  168,  177, 

211 

as  a  cause  of  fatty  degeneration 

of  heart,  299 

as  a  cause  of  mitral  incompetence, 

168,  278 

Anatomy  of  heart,  general  account  of,  i 
Aneurism  of  heart,  151,  291,  300,  306 
Angina  pectoris,  general  account  of,  310 

in  aortic  incompetence,  199 

in  fatty  disease  of  heart,  301 

in  fibroid  disease  of  heart,  306 

pseudo-,  311 

Aortic  area,  43 

incompetence,    general    account 

of,  195 

notch,  81 

orifice,  position  of,  4,  7 

size  of,  4 

second  sound,  45,  47 

accentuation  of,  48 

stenosis,  general  account  of,  207 


Aortitis,  26 

Aperients,  236,  283,  286,  298,  303 

Apex  beat,  character  of,  36 

— — —  displacement  of,  34,  35 

extent  of,  35 

position  of,  i,  6,  34 

Apoplexy,  pulmonary,  163 
Arcus  senilis,  301 
Arrhythmia,  331 
Arterial  tension,  78 

high,  causes  of,  79 

description  of,  85 

in  the  production  of  hyper- 
trophy, 259 

•  treatment  of,  239 

low,  causes  of,  78 

description  of,  85 

Asthenia,  cardiac,  330 

Asthma,  cardiac,  18,  25,  301,  306 

Asystole,  241,  266 

Atheroma,   20,   21,   80,   89,    160,    161, 

165,  204,  299,  312 
Auricle,  left,  dilatation  of,  266 

hypertrophy  of,  266 

impulse  of,  36 

position  of,  6 

right,  dilatation  of,  266 

hypertrophy  of,  266 

—  impulse  of,  36 

position  of,  6 

Auriculo-ventricular  sulcus,  7 
Auscultation,  general  account  of,  42 


B 


Bacteria  in  simple  endocarditis,  141 

in  malignant  endocarditis,  151 

in  myocarditis,  290 

Balfour  63,  318 
Bamberger,  124 

#  345 


346 


DISEASES  OF  THE  HEART 


Barie,  221 
Barr,  52 
Basch,  Von,  25 
Baths,  285,  341 

Bed,  rest  in,  127,  239,  241,  284,  287,  342 
Bouley,  315 
Bradycardia,  336 
Breath,  shortness  of,  18,  24 
Bristowe,  58,  335 

Broadbent,  Sir  \V.,  31,  52,  74,  132,  185, 
188,  191,  193,  219,  243,  246,  247, 

317 

Dr  John,  132 

Bronchitis,  18,  163,  170,  172 

Bruce,  Mitchell,  249 

Burns,  315 

Byrom  Bramwell,  140,  182,  212,  218 


Cactus  grandiflorus,  342 
Caffeine,  243,  244,  287 
Capillary  pulsation,  32,  201 
Cardiac  asthenia,  330 

asthma.  18,  25,  301,  306 

cycle,  9 

dulness,  deep,  6,  40 

superficial,  6,  39 

impulse,  11 

nerves,  12 

pain,  17,  327 

tonirs,  244 

Cardiogram  m  aortic  regurgitation,  98 

stenosis,  98 

mitral  regurgitation,  97 

• stenosis,  96 

Cardiograph,  general  account  of,  94 

Chauveau,  64 

Cheadle,  128,  144 

Cheyne-Stokes'  respiration,  18,  25,  172, 
301 

Chordee  tendineas,  rupture  of,  142,  151, 

Circulation  in  foetus,  103 
Climate,  236 
Compensation,  169,  198 

conditions  affecting,  162 

failure  of,  170,  198 

treatment  before  failure  of,  234 

after  failure  of,  238 

Congenital  affections  of  heart,  general 

account  of,  99 
Convallaria  majalis,  245,  287 
Corrigan's  pulse,  88 
Cough,  18 
Cyanosis,  23,  no,  226 


Ua  Costa,  328,  330,  343 
Death,    sudden,    131,    136,    173,    198, 
200,  209,  268,  298,  301,  306,  317 
Degeneration,  fatty,  of  heart,  298 

fibroid,  of  heart,  303 

parenchymatous,  of  heart,  294 

Development  of  heart,  99 

of  great  vessels,  100 

Diagnosis,  methods  of,  16 

physical  methods  of,  22 

Diastolic  murmurs,  55 

back  shock,  38 

Dicrotic  wave,  84 

Diet,  236,  281,  288 

Digitahs,  1 15,  245-7,  287 

Dilatation  of  heart,  general  account  of, 

253 

acute,  262 

Displacement  of  heart  and  apex  beat,  35 

Diuretics,  242,  286,  288 

Dreschfeld,  152 

Dropsy,  27,  173,  268 

Ductus  arteriosus,  102,  104,  106,  no 

Dulness,  cardiac,  deep,  6,  40 

superficial,  6,  39 

due  to  pericardial  effusion,   41, 

124 

Duroziez,  63,  132 
Dyspepsia,  18 
Dyspnoea,  causes  of,  24 


Eccentric  hypertrophy,  249,  258 
Effusion  into  pericardial  cavity,  41, 122-4 
Emaciation,  28,  185,  268 
EmboHsm,  18,  145,  154-6,  185,  251 
Endocardial  murmurs,  53,  54 
Endocarditis,  acute,  simple,  138 

malignant,  or  infective,  149 

chronic,  160 

Endocardium,  diseases  of,  138 

Epigastric  pulsation,  30 

Epileptiform  attacks,  338 

Epistaxis,  18,  172,  184,  199 

Ewart,  38,  123 

Exercise,  149,  235,  239,  281,  284,  285, 

303,  321,  341 
Exocardial  murmurs,  68 


Face,  expression  of,  23 

Fatty  degeneration  of  heart,  298 

infiltration  of  heart,  296 

Fibroid  disease  of  heart,  303 


DISEASES  OF  THE  HEART 


347 


Fingers,  clubbing  of,  23,  no,  174,  226 

Flint,  203 

Fluctuation,  38 

Foetal  circulation,  103 

Foster,  324 

Fox  well,  64 

Frankel  and  Saenger,  152 

Friction  sounds,  pericardial,  67,  121 

pleural,  68 

pleuro-pericardial,  68 

:  fremitus,  37,  121 

Functional  diseases  of  heart,  322 


Gairdner,  314 
Galabin,  12,  97,  98 
■  Gibson,  in 
Gilbert  and  Lyon,  151 
Great  vessels,  development  of,  102 


H 


H^MATEMESIS,   1 8,  1 72 

Hffimic  murmurs,  62 

Haemopericardium,  135 

Hremoptysis,  18,  183,  184 

Haemorrhoids,  19,  172 

Hamilton,  163 

Hayden,  64 

Heberden,  310,  315 

Head,  39,  327 

Heart,  abscess  of,  151,  290,  291 

aneurism  of,  15 1,  291,  300,  306 

dilatation  of,  249 

displacements  of,  35 

fatty  degeneration  of,  298 

infiltration  of,  296 

fibroid  disease  of,  303 

functional  disorders  of,  322 

hypertrophy  of,  249 

malformation  of,  108 

misplacements  of,  107 

nerves  of,  12 

new  growths  in,  307 

position  of,  i 

regulation  of  beat  of,  14,  325 

relation  of,  to  chest  wall,  5 

.rupture  of,  291,   297,   300,  301, 

306 

shape  of,  i 

size  and  weight  of,  2 

sounds  of,  12,  43 

topography  of,  5 

Heredity,  influence  of,  in  causation  of 
cardiac  disease,  22 


Herringham,  340 

History  of  patient  in  tetiology  of  heart 

disease,  21 
Huchard,  311 
Hydropericardium,  135 
Hypertrophy,  general  account  of,  249 


I 


Ice  bag,  use  of,  127,  148,  342 
Impulse  of  auricles,  36 
Impulse,  cardiac,  1 1 

diastolic,  36 

of  left  ventricle,  34 

of  right  ventricle,  36 

Infective  endocai'ditis,  149 
Insomnia,  19 

Inspection,  general  account  of,  22 
Interauricular  septum,  development  of, 
100 

malformation  of,  108 

Intermittent  action  of  heart,  331 
Interventricular    septum,    development 
of,  100 

malformation  of,  108 

rupture  of,  1 51,  291,  306 

sulcus,  position  of,  8 


J 


Jaundice,  24 

Jugular  veins,   distension   of,   32,    175, 
215,  219,  273 
pulsation  in,  32.  175,  215,  219, 

273 

Johnson,  52 


Leeches,  115,  127,  148,  242,  286 
Liver,    enlargement   of,    42,    172,    213, 
215,  219,  252 

examination  of,  42 

pulsation  of,  38,  215,  220,  273 


M 

Macalister,  4,  10 1 
Mackenzie,  220 
Maguire,  112,  124 
Mahomed,  83 
Malformation  of  heart,  108 

of  great  vessels,  109 

Massage,  115,  240,  244 


348 


DISEASES  OF  THE  HEART 


Micro-organisms  in  acute  simple  endo- 
carditis, 141 

malignant  endocarditis,  151, 

myocarditis,  290 

Milk  spots,  129 
Mitral  area,  43 

incompetence,    general    account 

of,  167 

opening,  position  of,  4,  6 

size  of,  4 

stenosis,  general  account  of,  181 

stages  of,  193 

valve,  4 

Morgagni,  23 

Morphia,  127,  243,  244,  288,  320 
Murmurs,  account  of,  53 

aortic,  59)  202,  210 

cardio-pulmonary,  68 

■ character  of,  60 

diastolic,  55 

differential  diagnosis  of  endo-  and 

exocardial,  70 

endocardial,  53 

exocardial,  53 

hsemic,  62 

mitral,  56,  175 

■ ■  mode  of  production  of,  54 

obstructive,  55 

organic,  54 

presystolic,  55,  58,  187,  203 

■ pulmonic,  59,  223,  227 

regurgitant,  55 

rhythm  of,  61 

• systolic,  55 

tricuspid,  60,  215,  219 

■  vascular,  53 

venous,  72 

Myocardium,  diseases  of,  248 
Myocarditis,  acute,  general  account  of, 

289 


N 

Nauheim,  240 

Nervous  supply  of  heart,  12 

New  growths  in  heart,  307 

in  pericardium,  137 

Nitrites.     See  Vaso-dilators 
Nutrition,  general  state  of,  in  cardiac 
disease,  28 


Occupation,  influence  of,  in  setiology 

of  cardiac  disease,  20 
GEdema,  27,  173,  268 
CErtel,  285 


Orthopnoea,  26 

Osier,  150,  3I5>.337 

Oxygen,  inhalation  of,  243,  288,  320 


Pain,  cardiac,  17,  327 
Pallor,  24 

Palpation,  general  account  of,  33 
Palpitation,  general  account  of,  328 
Paracentesis  pericardii,  128 
Paul,  211 

Peacock,  105,  112,  228 
Percussion,  general  account  of,  39 
Pericardial   adhesion,   general   account 
of,  129 

effusion,  41,  122-4 

Pericarditis,  acute,  general  account  of, 

116 
Pericardium,  diseases  of,  116 

shape  of,  i 

Petit,  185 

Physical  examination  of  heart,  22 
Physiognomy,  iii,  174,  185,  200,  209, 
214,  218,  222,  270,  272,  301,  306 
Pneumogastric  nerve,  12,  325 
Pneumopericardium,  136 
Potain,  51 
Prfficordium,  bulging  of,  28 

retraction  of,  29 

Predicrotic  wave,  81 

Presystolic  murmur,  55,  58,  187,  203 
Prognosis  in  acute  endocarditis,  147 

infective  endocarditis,  159 

myocarditis,  292 

in  angina  pectoris,  319 

in  chronic  valvular  affections,  230 

in  congenital  affections  of  heart, 

113 

in  dilatation  of  heart,  278 

■ in  fatty  degeneration  of  heart,  302 

•  infiltration  of  heart,  297 

in  fibroid  disease  of  heart,  307 

in  functional  disorders  of  heart, 

340 

in  hypertrophy  of  heart,  279 

■ in  pericardial  adhesion,  134 

Pulmonic  area,  44 

incompetence,    general    account 

of,  221 

orifice,  position  of,  4,  7    . 

size  of,  4 

•  second  sound,  45,  47,  49 

accentuation  of,  49 

stenosis,  general  account  of,  225 

Pulsation,  general  account  of  visible,  29 

—  of  palpable,  34 

Pulse,  account  of,  74 


DISEASES  OF  THE  HEART 


349 


Pulse,  collapsing,  88,  201 

Corrigan's,  88 

• high  tension,  78,  79,  85 

in  aneurism,  92 

in  aortic  incompetence,  88,  201 

stenosis,  89,  209 

• •  in  dilatation  of  heart,  87,  271,  274 

in  hypertrophy  of  heart,  87,  269, 

273 

in  mitral  incompetence,  91,  174 

stenosis,  91,  186 

low  tension,  78,  85 

recurrent,  80 

virtual  tension,  86,  317 

Pulsus  alternans,  77,  332 

bigeminus,  77,  332 

bisferiens,  90,  202 

paradoxus,  77,  133,  333 

trigeminus,  77,  332 

Purgatives,  115,  239,  242,  244,  283,  286 


QUAIN,  289,   304 


R 


Reduplication  of  heart  sounds,  51 
of  first  sound,  5 1 

of  second  sound,  52 

Relative  incompetence  of  aortic  valve, 
196 

of  mitral  valve,   168,  176,  278 

Rest,  127,  240,  241,  284,  287,  343 

Rheumatism,  21 

Rhythm  of  heart  sounds,  46 

Rokitansky,  100 

Rotch,  124,  128 

Roy  and  Adami,  98 

Rupture  of  heart,  291,  300,  301,  306 

of  valve,  195,  230 

Russell,  64 


Samways,  192 
Sansom,  52,  53,  64,  190 
Schott  treatment,  240,  285 
Semilunar  valves,  closure  of,  36 

developmental    anomalies    of, 

109 
Sex  as  affecting  prognosis,  232 


Sex,      influence     of,     in    setiology    in 

cardiac  affections,  20 
Sibson,  121,  123,  129 
Sleeplessness,  19,  120, 199,  243,  279,288 
Sounds  of  heart,  general  account  of,  43 
Sphygmogram,  general  account  of,  81 
Stimulants,    128,    149,    159,    287,   293, 

298,  307,  320,  342 
Stoke-Adams'  disease,  337 
Strophanthus,  244,  245,  282,  287,  343 
Sudden  death,  131,  136,  173,  198,  200, 

209,  268,  298,  300,  306,  317 
Sympathetic  nerves,  13,  325 
Symptomatology  in  cardiac  disease,  16 
Syncopal  attacks,    199,   209,  300,  301, 

306,  318,  336,  337,  338 
Syphilis,  21,  139,  195,  304,  308 
Systolic  murmurs,  55 


Tachycardia,  334 
Temperature,  ill 
Thompson,  103 
Thrills,  general  account  of,  37 
Tidal  wave,  83 
Tracheal  tugging,  38 
Treatment  of  acute  infective  endocar- 
ditis, 159 
Treatment  of  acute  myocarditis,  293 

simple  endocarditis,  148 

of  angina  pectoris,  319 

of  chronic  valvular  disease,  234 

of  congenital  affections  of  heart, 

"4 

of  dilatation  of  heart,  283 

of  fatty  degeneration  of  heart,  302 

infiltration  of  heart,  298 

of  fibroid  disease  of  heart,  307 

of  functional  disorders  of  heart, 

340 

of  hypertrophy  of  heart,  281 

■  (Ertel  285 

Schott,  240,  285 

Tricuspid  area,  44 

incompetence,    general    account 

of,  212 

orifice,  position  of,  4,  6 

size  of,  4 

stenosis,  general  account  of,  217 


U 


Urine  in  cardiac  disease,  19,  28 


350 


DISEASES  OF  THE  HEART 

V 


Vagus  nerve,  13,  325 
Valvular  lesions,  acute,  138 

chronic,  165 

Vascular  sounds,  general  account  of,  71 
Vaso-dilators,  239,  243,  287,  288,  320, 

321 
Veins,  jugular,  distension  of,  32,   175, 
215,  219,  273 
pulsation  in,  32,  175,  215,  219, 

273 
Venesection,  115,  128,  242,  286 
^^enous  murmurs,  72 
Ventricle,  left,  dilatation  of,  261 
first  sound  of,  45,  47 


Ventricle,  left  hypertrophy  of,  258 

impulse  of,  34 

position  of,  6 

right,  dilatation  of,  265 

first  sound  of,  45,  47,  49 

hypertrophy  of,  265 

■ ■ —  impulse  of,  36 

position  of,  6 

Vomiting,  127,  199,  279 


W 

Water-hammer  pulse,  88,  201 
Weichselbaum,  152 
Wilks,  134 


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